What makes UpToDate so powerful?

  • over 11000 topics
  • 22 specialties
  • 5,700 physician authors
  • evidence-based recommendations
See more sample topics
Find Patient Print
0 Find synonyms

Find synonyms Find exact match

Treatment of community-acquired pneumonia in adults who require hospitalization
UpToDate
Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate®
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
Treatment of community-acquired pneumonia in adults who require hospitalization
View in Chinese
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2017. | This topic last updated: Aug 10, 2017.

INTRODUCTION — Community-acquired pneumonia (CAP) is defined as an acute infection of the pulmonary parenchyma in a patient who has acquired the infection in the community, as distinguished from hospital-acquired (nosocomial) pneumonia (HAP).

CAP is a common and potentially serious illness [1-5]. It is associated with considerable morbidity and mortality, particularly in older adult patients and those with significant comorbidities. (See "Prognosis of community-acquired pneumonia in adults".)

The treatment of CAP in adults who require hospitalization will be reviewed here. A variety of other important issues related to CAP are discussed separately:

(See "Diagnostic approach to community-acquired pneumonia in adults".)

(See "Community-acquired pneumonia in adults: Assessing severity and determining the appropriate site of care".)

(See "Treatment of community-acquired pneumonia in adults in the outpatient setting".)

(See "Antibiotic and glucocorticoid studies for the treatment of community-acquired pneumonia in adults".)

(See "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults".)

Pneumonia in special populations, such as aspiration pneumonia, immunocompromised patients, HAP, and ventilator-associated pneumonia (VAP) are also discussed separately. (See "Aspiration pneumonia in adults" and "Pulmonary infections in immunocompromised patients" and "Treatment of hospital-acquired and ventilator-associated pneumonia in adults".)

MANAGEMENT OF HEALTHCARE-ASSOCIATED PNEUMONIA — Healthcare-associated pneumonia (HCAP) was included in prior hospital-acquired pneumonia (HAP) guidelines [6] (but not current HAP guidelines [7]) to identify patients thought to be at increased risk for multidrug-resistant (MDR) pathogens coming from community settings. HCAP referred to pneumonia acquired in healthcare facilities such as nursing homes, hemodialysis centers, and outpatient clinics or during a hospitalization within the past three months. The rationale for the separate designation of HCAP (and its association with HAP) was that patients with HCAP were thought to be at higher risk for MDR organisms. However, several studies have shown that many patients defined as having HCAP are not at high risk for MDR pathogens [8-10] and that this designation is not a good predictor of who will have an infection with an MDR organism [11]. Furthermore, although interaction with the healthcare system is potentially a risk for MDR pathogens, underlying patient characteristics (recent receipt of antimicrobials, comorbidities, functional status, and severity of illness) are important independent determinants of risk for MDR pathogens. In addition, there is no evidence to indicate that treating patients with HCAP according to the recommendations in HAP guidelines improves outcomes [12]. We feel that patients previously classified as having HCAP should be managed in a similar way to those with CAP (assessing risks for MDR organisms) because patients with HCAP frequently present from the community and are initially cared for in emergency departments.

DETERMINING THE APPROPRIATE SITE OF CARE — Determining whether a patient with community-acquired pneumonia (CAP) can be safely treated as an outpatient or requires admission to an observation unit, general medical ward, or higher acuity level of inpatient care, such as an intensive care unit (ICU), is an essential first step (algorithm 1). Severity of illness is the most critical factor in making this determination, but other factors should also be taken into account. The approach to site of care is discussed in greater detail elsewhere. (See "Community-acquired pneumonia in adults: Assessing severity and determining the appropriate site of care", section on 'Approach to site of care'.)

LIKELY PATHOGENS — Although a variety of bacterial pathogens can cause CAP, a limited number are responsible for the majority of cases; in addition, the causative organism is not identified in an appreciable proportion of patients (table 1 and table 2 and figure 1). (See "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults", section on 'Microbiology'.)

Medical ward — In patients who require hospitalization but not admission to an intensive care unit (ICU), the most frequently isolated pathogens are S. pneumoniae, respiratory viruses (eg, influenza, parainfluenza, respiratory syncytial virus, rhinovirus), and, less often, M. pneumoniae, H. influenzae, and Legionella spp (table 2).

Intensive care unit — The distribution is different in patients with CAP who require admission to an ICU. S. pneumoniae is most common, but Legionella, gram-negative bacilli, S. aureus, and influenza are also important (table 2). Community-associated methicillin-resistant S. aureus (MRSA) typically produces a necrotizing pneumonia with high morbidity and mortality. (See "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults", section on 'S. aureus'.)

Risk factors for Pseudomonas or drug-resistant pathogens

Gram-negative bacilli (including Pseudomonas) — Risk factors for CAP due to gram-negative bacilli include previous antibiotic therapy, recent hospitalization, immunosuppression, pulmonary comorbidity (eg, cystic fibrosis, bronchiectasis, or repeated exacerbations of chronic obstructive pulmonary disease that require frequent glucocorticoid and/or antibiotic use), probable aspiration, and multiple medical comorbidities (eg, diabetes mellitus, alcoholism) [2,13-15]. (See "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults", section on 'Gram-negative bacilli'.)

Methicillin-resistant Staphylococcus aureus — Risk factors for MRSA include gram-positive cocci in clusters seen on sputum Gram stain, known colonization with MRSA, risk factors for colonization with MRSA (eg, end-stage renal disease, contact sport participants, injection drug users, those living in crowded conditions, men who have sex with men, prisoners), recent influenza-like illness, antimicrobial therapy (particularly with a fluoroquinolone) in the prior three months, necrotizing or cavitary pneumonia, and presence of empyema.

Streptococcus pneumoniae — Risk factors for drug-resistant S. pneumoniae in adults include:

Age >65 years

Beta-lactam, macrolide, or fluoroquinolone therapy within the past three to six months

Alcoholism

Medical comorbidities

Immunosuppressive illness or therapy

Exposure to a child in a daycare center

Another risk factor is prior exposure to the healthcare setting such as from prior hospitalization or from residence in a long-term care facility.

Recent therapy or a repeated course of therapy with beta-lactams, macrolides, or fluoroquinolones are risk factors for pneumococcal resistance to the same class of antibiotic [16]. Thus, an antimicrobial agent from an alternative class is preferred for a patient who has recently received one of these agents.

The impact of discordant drug therapy, which refers to treatment of an infection with an antimicrobial agent to which the causative organism has demonstrated in vitro resistance, appears to vary with antibiotic class and possibly with specific agents within a class. Most studies have been performed in patients with S. pneumoniae infection and suggest that current levels of beta-lactam resistance generally do not cause treatment failure when appropriate agents (eg, amoxicillin, ceftriaxone, cefotaxime) and doses are used. Cefuroxime is a possible exception with beta-lactams, and there appears to be an increased risk of macrolide failure in patients with macrolide-resistant S. pneumoniae. (See "Antibiotic and glucocorticoid studies for the treatment of community-acquired pneumonia in adults", section on 'Outcomes with discordant drug therapy'.)

DIAGNOSTIC TESTING — The approach to diagnostic testing for hospitalized patients with CAP is summarized in the following table (table 3). In addition to the tests recommended in the table, we recommend testing for a specific organism when, based on clinical or epidemiologic data, pathogens that would not respond to usual empiric therapy are suspected (table 4) [2]. These include Legionella species, seasonal influenza, avian (H5N1, H7N9) influenza, Middle East respiratory syndrome coronavirus, community-acquired methicillin-resistant S. aureus (CA-MRSA), M. tuberculosis, and agents of bioterrorism such as anthrax. [17]. (See "Diagnostic approach to community-acquired pneumonia in adults" and "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults".)

Tests that are indicated (especially sputum Gram stain and culture and blood cultures) should ideally be performed before antibiotics have been started. However, initiation of treatment should not be delayed if it is not possible to obtain specimens immediately (eg, if the patient cannot produce a sputum specimen).

INITIAL EMPIRIC THERAPY — Antibiotic therapy is typically begun on an empiric basis, since the causative organism is not identified in an appreciable proportion of patients (table 1 and table 2) [2,4,5,18]. The clinical features and chest radiographic findings are not sufficiently specific to determine etiology and influence treatment decisions. (See "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults".)

The Gram stain of respiratory secretions can be useful for directing the choice of initial therapy if performed on a good quality sputum sample and interpreted by skilled examiners using appropriate criteria [2]. (See "Diagnostic approach to community-acquired pneumonia in adults", section on 'Sputum'.)

Antibiotic recommendations for hospitalized patients with CAP are divided by the site of care (medical ward or intensive care unit [ICU]). Most hospitalized patients are initially treated with an intravenous regimen. However, many patients without risk factors for severe pneumonia can be treated with oral therapy, especially with highly bioavailable agents such as the fluoroquinolones [19]. (See 'Medical ward' below and 'Intensive care unit' below.)

The selection of antimicrobial regimens for empiric therapy is based upon a number of factors, including:

The most likely pathogen(s). (See 'Likely pathogens' above.)

Clinical trials proving efficacy. (See "Antibiotic and glucocorticoid studies for the treatment of community-acquired pneumonia in adults".)

Risk factors for antimicrobial resistance. (See 'Risk factors for Pseudomonas or drug-resistant pathogens' above.)

Medical comorbidities, which may influence the likelihood of a specific pathogen and may be a risk factor for treatment failure.

Epidemiologic factors such as travel and concurrent epidemics (eg, Middle East respiratory syndrome coronavirus, avian influenza). (See "Middle East respiratory syndrome coronavirus: Virology, pathogenesis, and epidemiology" and "Epidemiology, transmission, and pathogenesis of avian influenza" and "Avian influenza A H7N9: Epidemiology, clinical manifestations, and diagnosis".)

Additional factors that may affect the choice of antimicrobial regimen include the potential for inducing antimicrobial resistance, pharmacokinetic and pharmacodynamic properties, safety profile, and cost [13].

Timing of antimicrobial initiation — We recommend that antimicrobials be administered as soon as possible after diagnosing CAP and before leaving the emergency department or clinic [2]. In patients with sepsis or septic shock, antibiotics should be started within one hour. (See "Evaluation and management of suspected sepsis and septic shock in adults", section on 'Empiric antibiotic therapy (first hour)'.)

Although several studies have suggested a survival benefit to early initiation of antibiotics, some experts have questioned whether it is an independent risk factor for this outcome. It is important to note, however, that a delay in antimicrobial therapy for seriously ill patients can adversely affect outcomes.

A 2016 systematic review included eight studies that evaluated time to initiation of antibiotics and noted that all of the studies were observational in design and therefore represented low-quality evidence [20]. The four studies that showed an association between early initiation of antibiotics and reduced mortality were the largest of the studies, and three of them included patients ≥65 years of age with greater illness severity at presentation. In contrast, the four smallest studies included adults of all ages with less severe illness and found no association between early antibiotic initiation and mortality.

Two of the larger studies showed the following findings:

In a retrospective study of 13,771 Medicare patients, antibiotic administration within four hours of hospital arrival was associated with reductions in mortality (6.8 compared with 7.4 percent with delay in antibiotics) and length of stay (0.4 days shorter) [21].

In a matched-propensity analysis of national data from the British Thoracic Society CAP audit that included 13,725 patients with CAP, adjusted 30-day inpatient mortality was lower for adults who first received antibiotics in four or fewer hours compared with more than four hours (adjusted odds ratio 0.84, 95% CI 0.74-0.94) [22]. However, it is not clear whether early antibiotics result in lower mortality or whether they are a marker for overall quality of care.

Medical ward

Without risk factors for resistance or Pseudomonas — For patients admitted to a general ward without risk factors for resistance, we suggest (table 5 and algorithm 2) [2,23]:

Combination therapy with ceftriaxone (1 to 2 g intravenously [IV] daily), cefotaxime (1 to 2 g IV every 8 hours), ceftaroline (600 mg IV every 12 hours), ertapenem (1 g IV daily), or ampicillin-sulbactam (1.5 to 3 g IV every 6 hours) plus a macrolide (azithromycin [500 mg IV or orally daily] or clarithromycin [500 mg twice daily] or clarithromycin XL [two 500 mg tablets once daily]). Doxycycline (100 mg orally or IV twice daily) may be used as an alternative to a macrolide. Oral administration of a macrolide or doxycycline is appropriate only for selected patients without evidence of or risk factors for severe pneumonia.

Monotherapy with a respiratory fluoroquinolone (levofloxacin 750 mg IV or orally daily or moxifloxacin 400 mg IV or orally daily or gemifloxacin 320 mg orally daily) is an appropriate alternative for patients who cannot receive a beta-lactam plus a macrolide.

Combination therapy with a beta-lactam plus a macrolide and monotherapy with a respiratory fluoroquinolone are of generally comparable efficacy for CAP overall. However, many observational studies have suggested that beta-lactam plus macrolide combination regimens are associated with better clinical outcomes in patients with severe CAP, possibly due to the immunomodulatory effects of macrolides. (See "Antibiotic and glucocorticoid studies for the treatment of community-acquired pneumonia in adults", section on 'Combination therapy'.)

Furthermore, the severity of adverse effects (including the risk for C. difficile infection) and the risk of selection for resistance in colonizing organisms are generally thought to be greater with fluoroquinolones than with the combination therapy regimens. For both of these reasons, we generally prefer combination therapy with a beta-lactam plus a macrolide rather than monotherapy with a fluoroquinolone. Nevertheless, cephalosporins and other antibiotic classes also increase the risk of C. difficile infection. (See "Clostridium difficile in adults: Epidemiology, microbiology, and pathophysiology", section on 'Antibiotic use'.)

Recent antibiotic use should also inform the decision about the most appropriate regimen; if the patient has used a beta-lactam in the prior three months, a fluoroquinolone should be chosen, if possible, and vice versa. (See 'Risk factors for Pseudomonas or drug-resistant pathogens' above.)

The approach to patients with penicillin allergy and/or cephalosporin allergy is presented below. (See 'Penicillin and cephalosporin allergy' below.)

With risk factors for resistance or Pseudomonas — If the patient has risk factors for Pseudomonas or drug-resistant pathogens, such as methicillin-resistant S. aureus (MRSA), coverage for these organisms should be included, as discussed below. (See 'With risk factors for Pseudomonas or resistant gram-negative bacilli' below and 'With risk factors for MRSA' below.)

Penicillin and cephalosporin allergy — For penicillin-allergic patients, the type and severity of reaction should be assessed. Individuals with a past reaction to penicillin that was mild (not Stevens Johnson syndrome, toxic epidermal necrolysis, or drug reaction with eosinophilia and systemic symptoms [DRESS]) and did not have features of an IgE-mediated reaction can receive a broad-spectrum (third- or fourth-generation) cephalosporin or carbapenem safely.

Skin testing is indicated in some situations. Indications and strategies for skin testing are reviewed elsewhere. (See "Choice of antibiotics in penicillin-allergic hospitalized patients".)

For penicillin-allergic patients, if a skin test is positive or if there is significant concern to warrant avoidance of a cephalosporin or carbapenem, an alternative regimen should be given.

The appropriate regimen depends upon several factors, including the risk of Pseudomonas infection (algorithm 2):

Patients without risk factors for Pseudomonas infection who are admitted to the general medical ward can be treated with a respiratory fluoroquinolone (levofloxacin 750 mg IV or orally daily; moxifloxacin 400 mg IV or orally daily; gemifloxacin 320 mg orally daily).

Monotherapy with tigecycline is another alternative, but it should be limited to patients intolerant of both beta-lactams and fluoroquinolones since it has been associated with increased mortality [24-26].

Most patients with risk factors for Pseudomonas infection who are admitted to the general medical ward should receive levofloxacin (750 mg IV or orally daily) plus aztreonam (2 g IV every 8 hours) plus an aminoglycoside (gentamicin, tobramycin, or amikacin). Patients with a prior life-threatening or anaphylactic reaction (involving urticaria, bronchospasm, and/or hypotension) to ceftazidime should not be given aztreonam unless evaluated by an allergy specialist because of the possibility of cross-reactivity. Such patients can receive levofloxacin plus an aminoglycoside for antipseudomonal coverage in the interim.

These regimens do not include an agent for community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). Agents for patients at risk for CA-MRSA are discussed below. (See 'With risk factors for MRSA' below.)

Regimens for patients admitted to the ICU are presented below. (See 'Penicillin and cephalosporin allergy' below.)

Influenza therapy — Antiviral treatment is recommended as soon as possible for all persons with suspected or confirmed influenza requiring hospitalization or who have progressive, severe, or complicated influenza infection, regardless of previous health or vaccination status [27]. (See "Treatment of seasonal influenza in adults".)

Intensive care unit — Patients requiring admission to an ICU are more likely to have risk factors for resistant pathogens, including CA-MRSA and Legionella spp [2,28]. Establishing an etiologic diagnosis is particularly important in such patients. (See "Diagnostic approach to community-acquired pneumonia in adults".)

The approach to therapy is summarized in the following algorithm (algorithm 3) and discussed below.

Without risk factors for resistance or Pseudomonas — In patients without risk factors for or microbiologic evidence of P. aeruginosa or MRSA, we recommend intravenous combination therapy with a potent anti-pneumococcal beta-lactam (ceftriaxone 1 to 2 g daily, cefotaxime 1 to 2 g every 8 hours, ceftaroline 600 mg every 12 hours, or ampicillin-sulbactam 3 g every 6 hours) plus an advanced macrolide (azithromycin 500 mg daily) (table 5). Although the optimal doses of the beta-lactams (ceftriaxone, cefotaxime, ampicillin-sulbactam) have not been studied adequately, we favor the higher doses, at least initially, until the minimum inhibitory concentrations (MICs) against possible isolates (eg, S. pneumoniae) are known.

For the second agent, an alternative to azithromycin is a respiratory fluoroquinolone (levofloxacin 750 mg daily or moxifloxacin 400 mg daily). Regimens containing either a macrolide or fluoroquinolone have been generally comparable in clinical trials. However, many observational studies have suggested that macrolide-containing regimens are associated with better clinical outcomes for patients with severe CAP, possibly due to immunomodulatory effects of macrolides. For this reason, we generally favor a macrolide-containing regimen in this setting, unless there is a specific reason to avoid macrolides, such as patient allergy or intolerance. (See "Antibiotic and glucocorticoid studies for the treatment of community-acquired pneumonia in adults", section on 'Combination therapy'.)

Furthermore, the severity of adverse effects (including the risk for C. difficile infection) and the risk of selection for resistance in colonizing organisms are generally thought to be greater with fluoroquinolones than with other antibiotic classes. Nevertheless, cephalosporins and other antibiotic classes also increase the risk of C. difficile infection. (See "Clostridium difficile in adults: Epidemiology, microbiology, and pathophysiology", section on 'Antibiotic use'.)

Recent antibiotic use should also inform the decision about the most appropriate regimen. (See 'Risk factors for Pseudomonas or drug-resistant pathogens' above.)

With risk factors for Pseudomonas or resistant gram-negative bacilli — In patients who may be infected with P. aeruginosa or other resistant gram-negative pathogens (particularly those with structural lung abnormalities [eg, bronchiectasis], chronic obstructive pulmonary disease [COPD] and frequent antimicrobial or glucocorticoid use, and/or gram-negative bacilli seen on sputum Gram stain), empiric therapy should include agents effective against pneumococcus, P. aeruginosa, and Legionella spp. However, if P. aeruginosa or another resistant gram-negative pathogen is not isolated, coverage for these organisms should be discontinued. Acceptable regimens include combination therapy with an antipseudomonal/antipneumococcal beta-lactam antibiotic and an antipseudomonal fluoroquinolone, such as the following regimens:

Piperacillin-tazobactam (4.5 g every six hours) or

Imipenem (500 mg IV every six hours) or

Meropenem (1 g every eight hours) or

Cefepime (2 g every eight hours) or

Ceftazidime (2 g every eight hours)

PLUS

Ciprofloxacin (400 mg every eight hours) or

Levofloxacin (750 mg daily)

The fluoroquinolones may be administered orally when the patient is able to take oral medications, as they have excellent bioavailability. The dose of levofloxacin is the same when given intravenously and orally, while the dose of ciprofloxacin is 750 mg orally twice daily. (See "Fluoroquinolones", section on 'Pharmacokinetics'.)

With risk factors for MRSA — Empiric therapy for community-acquired methicillin-resistant S. aureus (CA-MRSA) should be given to hospitalized patients with septic shock or respiratory failure requiring mechanical ventilation. We also suggest empiric therapy of MRSA in patients with CAP who have any of the following risk factors: gram-positive cocci in clusters seen on sputum Gram stain, known colonization with MRSA, risk factors for colonization with MRSA (eg, end-stage renal disease, contact sport participants, injection drug users, those living in crowded conditions, men who have sex with men, prisoners), recent influenza-like illness, antimicrobial therapy (particularly with a fluoroquinolone) in the prior three months, necrotizing or cavitary pneumonia, or presence of empyema.

In such patients, we recommend treatment for MRSA with the addition of vancomycin (15 mg/kg IV every 12 hours, adjusted to a trough level of 15 to 20 mcg/mL and for renal function; in seriously ill patients, a loading dose of 25 to 30 mg/kg may be given) or linezolid (600 mg IV every 12 hours) until the results of culture and susceptibility testing are known. Clindamycin (600 mg IV or orally three times daily) may be used as an alternative to vancomycin or linezolid if the isolate is known to be susceptible. Ceftaroline is active against most strains of MRSA but is not FDA approved for pneumonia caused by S. aureus. Linezolid may be given orally when the patient is able to receive oral medications. If MRSA is not isolated, coverage for this organism should be discontinued. (See 'Community-acquired MRSA' below.)

The combination of vancomycin and piperacillin-tazobactam has been associated with acute kidney injury. In patients who require an anti-MRSA agent and an antipseudomonal/antipneumococcal beta-lactam, options include using a beta-lactam other than piperacillin-tazobactam (eg, cefepime or ceftazidime) or, if piperacillin-tazobactam is favored, using linezolid instead of vancomycin. (See "Vancomycin: Parenteral dosing, monitoring, and adverse effects in adults", section on 'Nephrotoxicity'.)

Penicillin and cephalosporin allergy — As noted above, for penicillin-allergic patients, the type and severity of reaction should be assessed. (See 'Penicillin and cephalosporin allergy' above.)

For penicillin-allergic patients, if a skin test is positive or if there is significant concern to warrant avoidance of a cephalosporin or carbapenem, an alternative regimen should be given.

The appropriate regimen depends upon several factors, including the risk of Pseudomonas infection (algorithm 3):

For most patients without risk factors for Pseudomonas infection who are admitted to the ICU, the beta-lactams recommended for those without penicillin allergy should be replaced with a respiratory fluoroquinolone plus aztreonam (2 g IV every 8 hours).

Ceftazidime and aztreonam have similar side chain groups, and cross-reactivity between the two drugs is variable. Patients with a prior life-threatening or anaphylactic reaction (involving urticaria, bronchospasm, and/or hypotension) to ceftazidime should not be given aztreonam unless evaluated by an allergy specialist because of the possibility of cross-reactivity. Such patients can receive levofloxacin plus an aminoglycoside for antipseudomonal coverage in the interim.

The prevalence of cross-sensitivity between ceftazidime and aztreonam has been estimated at <5 percent of patients, based upon limited data. A reasonable approach in those with mild past reactions to ceftazidime (eg, uncomplicated maculopapular rash) would involve informing the patient of the low risk of cross-reactivity and administering aztreonam with a graded challenge (1/10 dose followed by a one-hour period of observation; if no symptoms, give the full dose followed by another hour of observation). (See "Cephalosporin-allergic patients: Subsequent use of cephalosporins and related antibiotics", section on 'Use of carbapenems and monobactams' and "An approach to the patient with drug allergy", section on 'Graded challenge'.)

Most patients with risk factors for Pseudomonas infection who are admitted to the ICU should receive levofloxacin (750 mg IV or orally daily) plus aztreonam (2 g IV every 8 hours) plus an aminoglycoside (gentamicin, tobramycin, or amikacin). Patients with a prior life-threatening or anaphylactic reaction (involving urticaria, bronchospasm, and/or hypotension) to ceftazidime should not be given aztreonam unless evaluated by an allergy specialist because of the possibility of cross-reactivity. Such patients can receive levofloxacin plus an aminoglycoside for antipseudomonal coverage in the interim.

These regimens do not include an agent for CA-MRSA. Agents for patients at risk for CA-MRSA are discussed below. (See 'Community-acquired MRSA' below.)

Adjunctive glucocorticoids — We generally give glucocorticoids to severely ill patients (ie, patients admitted to the ICU), especially to those with a high systemic inflammatory response (C-reactive protein >15 mg/dL [>150 mg/L]) [29,30]. We are less likely to give glucocorticoids to patients at increased risk of adverse effects due to glucocorticoids (eg, recent upper gastrointestinal bleeding).

In patients at elevated risk of adverse effects, clinicians should make the decision about whether to give glucocorticoids on a case-by-case basis. There is limited evidence that infections caused by certain pathogens (influenza virus, Aspergillus spp) may be associated with worse outcomes in the setting of glucocorticoid use [31,32]; given these concerns, we avoid adjunctive glucocorticoids if one of these pathogens is detected. (See "Treatment and prevention of pandemic H1N1 influenza ('swine influenza')", section on 'Effect of glucocorticoids'.)

The rationale for giving glucocorticoids as adjunctive therapy to antibiotics in hospitalized patients with CAP is to reduce the inflammatory response to pneumonia, which is likely to contribute to the morbidity of the disease.

When we give glucocorticoids to patients who are unable to take oral medications, we use methylprednisolone 0.5 mg/kg IV every 12 hours. For patients who can take oral medications, we use prednisone 50 mg orally daily. We continue glucocorticoids for a total of five days.

We generally use glucocorticoids in ICU patients but not in patients admitted to medical wards for the following reasons:

A meta-analysis showed only a modest mortality benefit in hospitalized patients with CAP who received glucocorticoids, but severely ill patients are most likely to derive a benefit from glucocorticoids; the reason for this is that severely ill patients have a higher baseline risk of poor outcomes and would therefore be expected to have a higher absolute risk reduction with glucocorticoids [33].

CAP is caused by many different pathogens, but, in most patients, the pathogen is not identified. Little is known about whether there are varying harms or benefits of glucocorticoids depending upon the causative pathogen. As noted above, we avoid glucocorticoids when influenza or Aspergillus is the causative pathogen, as glucocorticoids may be associated with worse outcomes when one of these organisms is implicated [31,32].

Many of the randomized trials included in the meta-analysis mentioned above excluded patients at increased risk of adverse effects from glucocorticoids, including immunocompromised patients, pregnant women, patients who had gastrointestinal bleeding within the past three months, and patients at increased risk of neuropsychiatric side effects [33]. The incidence of some of these adverse effects may have therefore been underestimated. On the other hand, none of these conditions are absolute contraindications to glucocorticoid use. We consider the potential risks and benefits of glucocorticoids in each patient and decide whether to give adjunctive glucocorticoids when the potential benefits outweigh the potential risks.

It should be noted that different glucocorticoid formulations (eg, IV methylprednisolone, oral prednisone), doses, and routes of administration were used in different trials, and the optimal regimen is unknown. In most trials, patients received glucocorticoids for five to seven days, but it is possible that a longer duration is required for maximum benefit to be achieved.

The evidence supporting the adjunctive use of glucocorticoids is discussed in greater detail separately. (See "Antibiotic and glucocorticoid studies for the treatment of community-acquired pneumonia in adults", section on 'Adjunctive glucocorticoids'.)

Influenza therapy — Antiviral treatment is recommended as soon as possible for all persons with suspected or confirmed influenza requiring hospitalization or who have progressive, severe, or complicated influenza infection, regardless of previous health or vaccination status [27]. (See "Treatment of seasonal influenza in adults".)

SUBSEQUENT MANAGEMENT

Clinical response to therapy — With appropriate antibiotic therapy, some improvement in the patient's clinical course is usually seen within 48 to 72 hours (table 6). Patients who do not demonstrate some clinical improvement within 72 hours are considered nonresponders.

The time course of the clinical response to therapy is illustrated by the following observations:

In a prospective, multicenter cohort study of 686 adults hospitalized with CAP, the median time to becoming afebrile was two days when fever was defined as 38.3ºC (101ºF), and three days when defined as either 37.8ºC (100ºF) or 37.2ºC (99ºF) [34]. However, fever in patients with lobar pneumonia may take three days or longer to improve.

In a second prospective, multicenter trial of 1424 patients hospitalized with CAP, the median time to stability (defined as resolution of fever, heart rate <100 beats/min, respiratory rate <24 breaths/min, systolic blood pressure of ≥90 mmHg, and oxygen saturation ≥90 percent for patients not receiving prior home oxygen) was four days [35].

Although a clinical response to appropriate antibiotic therapy is seen relatively quickly, the time to resolution of all symptoms and radiographic findings is more prolonged. With pneumococcal pneumonia, for example, the cough usually resolves within eight days, and auscultatory crackles clear within three weeks. (See "Pneumococcal pneumonia in adults".)

In addition, as many as 87 percent of inpatients with CAP have persistence of at least one pneumonia-related symptom (eg, fatigue, cough with or without sputum production, dyspnea, chest pain) at 30 days compared with 65 percent by history in the month prior to the onset of CAP [36]. Patients should be told that some symptoms can last this long so that they are able to set reasonable expectations for their clinical course. (See "Prognosis of community-acquired pneumonia in adults", section on 'Mortality and symptom resolution'.)

Issues relating to nonresolving pneumonia are discussed in detail separately. (See "Nonresolving pneumonia".)

Radiographic response — Radiographic improvement typically lags behind the clinical response [37-40]. This issue was addressed in a prospective multicenter trial of 288 patients hospitalized for severe CAP; the patients were followed for 28 days in order to assess the timing of resolution of chest radiograph abnormalities [37]. The following findings were noted:

At day 7, 56 percent had clinical improvement but only 25 had resolution of chest radiograph abnormalities.

At day 28, 78 percent had attained clinical cure but only 53 percent had resolution of chest radiograph abnormalities. The clinical outcomes were not significantly different between patients with and without deterioration of chest radiograph findings during the follow-up period.

Delayed radiographic resolution was independently associated with multilobar disease.

In other studies, the timing of radiologic resolution of the pneumonia varied with patient age and the presence of underlying lung disease [38,39]. The chest radiograph usually cleared within four weeks in patients younger than 50 years of age without underlying pulmonary disease. In contrast, resolution could be delayed for 12 weeks or more in older individuals and in those with underlying lung disease.

Patients who respond to therapy

Narrowing therapy — If a pathogen has been established based upon reliable microbiologic methods and there is no laboratory or epidemiologic evidence of coinfection, we recommend narrowing therapy ("de-escalation") to target the specific pathogen in order to avoid antibiotic overuse. The results of diagnostic studies that provide identification of a specific etiology within 24 to 72 hours can be useful for guiding continued therapy. (See "Diagnostic approach to community-acquired pneumonia in adults".)

Pathogen-specific therapy for specific organisms is summarized in the table and discussed in greater detail separately (table 7). (See "Pneumococcal pneumonia in adults" and "Mycoplasma pneumoniae infection in adults" and "Pneumonia caused by Chlamydia pneumoniae in adults" and "Treatment and prevention of Legionella infection" and "Pseudomonas aeruginosa pneumonia" and "Clinical features, diagnosis, and treatment of Klebsiella pneumoniae infection" and "Treatment of seasonal influenza in adults".)

In a randomized trial, pathogen-directed treatment (PDT) was compared with empiric broad-spectrum antibiotic treatment (EAT) in 262 hospitalized patients with CAP [41]. PDT was based upon microbiologic studies (rapid diagnostic tests) or clinical presentation; EAT patients received a beta-lactam-beta-lactamase inhibitor plus erythromycin or, if admitted to the intensive care unit (ICU), ceftazidime and erythromycin. Overall, clinical outcomes (length of stay, 30-day mortality, fever resolution, and clinical failure) were the same for both groups. Adverse events were more frequent in the EAT group but were primarily related to the specific antimicrobial choice (ie, erythromycin).

Switching to oral therapy — Patients requiring hospitalization for CAP are generally begun on intravenous therapy. They can be switched to oral therapy when they are improving clinically, hemodynamically stable, able to take oral medications, and have a normally functioning gastrointestinal tract (algorithm 4) [2].

If the pathogen has been identified, the choice of oral antibiotic therapy is based upon the susceptibility profile (table 7). If a pathogen is not identified, the choice of antibiotic for oral therapy is usually either the same as the intravenous antibiotic or in the same drug class. If S. aureus, Pseudomonas, or a resistant gram-negative bacillus have not been isolated from a good quality sputum specimen, then empiric therapy for these organisms is not necessary. (See "Sputum cultures for the evaluation of bacterial pneumonia".)

The choice of oral regimen depends on the risk of drug-resistant S. pneumoniae and on the initial IV regimen:

In patients who are treated with the combination of an intravenous beta-lactam and a macrolide who have risk factors for drug-resistant S. pneumoniae (DRSP), we replace the intravenous beta-lactam with high-dose amoxicillin (1 g orally three times daily) to complete the course of therapy. When DRSP is not a concern, amoxicillin can be given at a dose of 500 mg orally three times daily or 875 mg orally twice daily. In patients who have already received 1.5 g of azithromycin who do not have Legionella pneumonia, we do not continue atypical coverage. Conversely, in patients who have not received 1.5 g of azithromycin, we give amoxicillin in combination with a macrolide or doxycycline. An alternative for patients without risk factors for DRSP is to give a macrolide or doxycycline alone to complete the course of therapy. The dosing for macrolides and doxycycline is (see 'Risk factors for Pseudomonas or drug-resistant pathogens' above and "Treatment of community-acquired pneumonia in adults in the outpatient setting", section on 'Treatment regimens'):

Azithromycin – 500 mg once daily

Clarithromycin – 500 mg twice daily

Clarithromycin XL – Two 500 mg tablets (1000 mg) once daily

Doxycycline – 100 mg twice daily

Patients who are treated initially with an IV respiratory fluoroquinolone can switch to the oral formulation of the same agent (eg, levofloxacin 750 mg once daily or moxifloxacin 400 mg once daily) to complete the course of therapy.

The duration of therapy is discussed below. (See 'Duration of therapy' below.)

Two prospective observational studies in 253 patients evaluated the clinical outcome of an early switch from intravenous to oral therapy in the treatment of CAP [42,43]. Patients met the following criteria prior to switching: resolution of fever, improvement in respiratory function, decrease in white blood cell count, and normal gastrointestinal tract absorption. Only two patients failed treatment, and the protocol was associated with high patient satisfaction [43].

Similar outcomes were noted in a multicenter randomized trial in the Netherlands of 265 patients with CAP (mean age 70) admitted to non–intensive care wards [44]. Patients were initially treated with three days of intravenous antibiotics and, when clinically stable, were assigned either to oral antibiotics to complete a total course of 10 days or to a standard regimen of 7 days of intravenous antibiotics. There was no difference in 28-day mortality (4 versus 2 percent) or clinical cure rate (83 versus 85 percent), while the length of hospital stay was reduced in the oral switch group by a mean of 1.9 days (9.6 versus 11.5 days).

In another randomized trial, a three-step pathway that involved early mobilization of patients in combination with the use of objective criteria for switching to an oral antibiotic regimen and for deciding on hospital discharge was compared to usual care [45]. The median length of stay was significantly shorter in the patients who were assigned to the three-step pathway (3.9 versus 6.0 days). In addition, the median duration of intravenous antibiotics was significantly shorter in the patients who were assigned to the three-step pathway (2.0 versus 4.0 days). More patients assigned to usual care experienced adverse drug reactions (4.5 versus 16 percent). No significant differences were observed in the rate of readmission, the case-fatality rate, or patients' satisfaction with care.

Documentation of pneumococcal bacteremia does not appear to alter the effect of switching to oral therapy early (no clinical failures in 18 such patients switched based upon the above criteria in one report) [46].

Duration of hospitalization — Hospital discharge is appropriate when the patient is clinically stable from the pneumonia, can take oral medication, has no other active medical problems, and has a safe environment for continued care; patients do not need to be kept overnight for observation following the switch. Early discharge based on clinical stability and criteria for switch to oral therapy is encouraged to reduce unnecessary hospital costs and hospital-associated risks, including iatrogenic complications and greater risk for antimicrobial resistance.

Several studies have shown that it is not necessary to observe stable patients overnight after switching from intravenous to oral therapy, although this has been common practice [2,47,48]. As an example, a retrospective review of the United States Medicare National Pneumonia Project database compared outcomes between patients hospitalized for CAP who were not (n = 2536) and were (n = 2712) observed overnight after switching to oral therapy [48]. The following findings were noted:

No significant difference in 14-day hospital readmission rate (7.8 versus 7.2 percent)

No significant difference in the 30-day mortality rate (5.1 versus 4.4 percent)

The importance of clinical stability at discharge was illustrated in a prospective observational study of 373 Israeli patients discharged with a diagnosis of CAP [49]. On the last day of hospitalization, seven parameters of instability were evaluated (temperature >37.8ºC [100ºF], respiratory rate [RR] >24 breaths/min, heart rate [HR] >100 beats/min, systolic blood pressure [SBP] ≤90 mmHg, oxygen saturation <90 percent on room air, inability to receive oral nutrition, and change of mental status from baseline). At 60 days post discharge, patients with at least one parameter of instability at discharge were significantly more likely to have died or required readmission than patients with no parameters of instability (death rates, 14.6 versus 2.1 percent; readmission rates, 14.6 versus 6.5 percent).

As noted above, in one trial, a three-step pathway that involved early mobilization of patients in combination with the use of objective criteria for switching to an oral antibiotic regimen and for deciding on hospital discharge was compared with usual care [45]. The median length of stay was significantly shorter in the patients who were assigned to the three-step pathway (3.9 versus 6.0 days).

Duration of therapy — Based upon the available data, we agree with the recommendation of the IDSA/ATS guidelines that patients with CAP should be treated for a minimum of five days [2]. Thus, the recommended duration for patients with good clinical response within the first two to three days of therapy is five to seven days total. Data that support this recommendation are presented separately. (See "Antibiotic and glucocorticoid studies for the treatment of community-acquired pneumonia in adults", section on 'Duration of therapy'.)

Before stopping therapy, the patient should be afebrile for 48 to 72 hours, breathing without supplemental oxygen (unless required for preexisting disease), and have no more than one clinical instability factor (defined as HR >100 beats/min, RR >24 breaths/min, and SBP ≤90 mmHg) (algorithm 5) [2].

A longer duration of therapy is needed in the following settings:

If the initial therapy was not active against the subsequently identified pathogen. (See 'Clinical response to therapy' above.)

If extrapulmonary infection is identified (eg, meningitis or endocarditis).

If the patient has pneumonia caused by P. aeruginosa, S. aureus, or Legionella spp or pneumonia caused by some unusual and less common pathogens (eg, Burkholderia pseudomallei, fungus).

If the patient has necrotizing pneumonia, empyema, or lung abscess [50].

The duration of therapy in these patients should be individualized based upon the clinical response to treatment and patient comorbidities. For the treatment of MRSA pneumonia without metastatic infection, duration will vary, with a recommendation of 7 to 21 days depending upon the extent of infection [51]. A 7- to 10-day course is generally appropriate for patients who respond within 72 hours. In a study of ventilator-associated pneumonia (VAP) due to MRSA (although not likely due to the USA 300 strain that causes community-acquired MRSA pneumonia), 8 days of therapy was as effective as 15 days of therapy [52].

Switching from IV to oral therapy is discussed above. (See 'Switching to oral therapy' above.)

Patients are often treated with antibiotics for longer than necessary. Antimicrobial stewardship programs can help to shorten the duration of antibiotics and narrow the spectrum of antibiotics [53]. (See "Antimicrobial stewardship in hospital settings".)

We favor the use of procalcitonin to help guide the duration of therapy. Procalcitonin has been evaluated for guiding the decision to stop antibiotics since the procalcitonin level appears to correlate with the likelihood of a bacterial infection [54]. The use of procalcitonin-guided algorithms in patients with CAP appears to be effective at reducing the duration of antibiotics without sacrificing patient safety. In a 2012 Cochrane meta-analysis of 14 randomized trials in which an algorithm was used to aid with the decision to discontinue antibiotics in patients who were unlikely to have bacterial pneumonia, no difference in mortality was seen among those whose care was guided by the procalcitonin result and those whose care was not [55]. In most of the trials, among clinically stable patients, a procalcitonin concentration <0.25 mcg/L led to a recommendation to discontinue antibiotics, and a concentration <0.1 mcg/L led to a strong recommendation to discontinue antibiotics. The uses of procalcitonin in patients suspected of having CAP is discussed in detail separately. (See "Diagnostic approach to community-acquired pneumonia in adults", section on 'Procalcitonin and CRP'.)

Clinical follow-up after discharge — Patients who have been discharged from the hospital with CAP should have a follow-up visit, usually within one week. In addition, a later visit is often indicated to assess for resolution of pneumonia.

Follow-up chest radiograph — Most patients with clinical resolution after treatment do not require a follow-up chest radiograph. We perform chest radiograph at 7 to 12 weeks following treatment in patients >50 years of age, particularly in males and smokers in this age group [56].

Chest radiograph is performed in this relatively higher risk population in order document resolution of the pneumonia and to exclude underlying diseases, particularly malignancy. In a large population-based cohort study of patients with CAP, new lung cancer was diagnosed within 90 days of CAP in 1.1 percent and within 5 years in 2.3 percent [57]. On multivariate analysis, the characteristic most strongly associated with lung cancer was age >50 years (adjusted hazard ratio [aHR] 19.0, 95% CI 5.7-63.6); other risk factors were male sex (aHR 1.8, 95% CI 1.1-2.9) and smoking (aHR 1.7, 95% CI 1.0-3.0).

SPECIFIC CONSIDERATIONS

Community-acquired MRSA — As discussed above, empiric therapy for community-acquired methicillin-resistant S. aureus (CA-MRSA) should be given to hospitalized patients with septic shock or respiratory failure requiring mechanical ventilation. It should also be given to those with risk factors for MRSA. (See 'Methicillin-resistant Staphylococcus aureus' above.)

Although data regarding the therapy of pneumonia caused by CA-MRSA are limited, a randomized trial showed superiority in clinical outcomes, but not mortality, of linezolid compared with vancomycin in hospital-acquired or healthcare-associated pneumonia caused by MRSA [58]. In contrast, in a meta-analysis of nine randomized trials of patients with hospital-acquired pneumonia that compared linezolid and vancomycin, there were no differences in mortality or clinical response [59]. The treatment of MRSA pneumonia is discussed in detail separately. (See "Treatment of hospital-acquired and ventilator-associated pneumonia in adults", section on 'Methicillin-resistant Staphylococcus aureus'.)

Although community-acquired MRSA is typically susceptible to more antibiotics than hospital-acquired MRSA, it appears to be more virulent [60]. CA-MRSA often causes a necrotizing pneumonia [61,62]. The strain causing CA-MRSA is known as "USA 300" and the gene for Panton Valentine Leukocidin (PVL) characterizes this strain [63-67]. However, an animal study suggests that the virulence of CA-MRSA strains is probably not due to PVL [68]. In addition, one study of patients with hospital-acquired pneumonia due to MRSA observed that the severity of infection and clinical outcome was not influenced by the presence of the PVL gene [69]. It is possible that other cytolytic toxins play a role in the pathogenesis of CA-MRSA infections. Vancomycin does not decrease toxin production, whereas linezolid has been shown to reduce toxin production in experimental models [70,71]. (See "Virulence determinants of community-acquired methicillin-resistant Staphylococcus aureus".)

One concern with vancomycin is the increasing MICs of MRSA that have emerged in recent years, which may reduce the efficacy of vancomycin in pulmonary infection. In patients with a MRSA isolate with an increased vancomycin MIC (>2 mcg/mL), we prefer linezolid. Vancomycin-intermediate and vancomycin-resistant S. aureus infection is discussed in greater detail separately. (See "Staphylococcus aureus bacteremia with reduced susceptibility to vancomycin".)

When vancomycin is used, trough concentrations should be monitored in order to ensure that a target trough concentration between 15 and 20 mcg/mL is achieved. There may be important differences in potency and toxicity based on the supply source of generic formulations of vancomycin [72]. (See "Vancomycin: Parenteral dosing, monitoring, and adverse effects in adults".)

Factors associated with rapid mortality include infection with influenza, the need for ventilator or inotropic support, onset of respiratory distress syndrome, hemoptysis, and leukopenia. In a report of 51 cases of CAP caused by S. aureus (79 percent of which were MRSA), 39 percent had a white blood cell [WBC] count <4000/microL, and this finding was associated with a poor prognosis. In contrast, a WBC >10,000/microL appeared to be protective [73].

If a sputum culture reveals methicillin-susceptible S. aureus (MSSA), therapy should be changed to nafcillin (2 g IV every four hours) or oxacillin (2 g IV every four hours) (table 7).

Atypical bacteria — The value of providing empiric coverage for atypical pathogens (eg, M. pneumoniae, C. pneumoniae, Legionella spp) is debated [74,75]. One reason for this is that testing for M. pneumoniae and C. pneumoniae is not usually done and, until 2012, there were no US Food and Drug Administration (FDA)-cleared polymerase chain reaction tests to detect them. Thus, their role in an individual case or in population-based studies is not well elucidated. (See "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults", section on 'Common pathogens' and "Diagnostic approach to community-acquired pneumonia in adults", section on 'Chlamydia pneumoniae' and "Diagnostic approach to community-acquired pneumonia in adults", section on 'Mycoplasma pneumoniae'.)

The evidence regarding empiric therapy for atypical bacteria is presented separately. (See "Antibiotic and glucocorticoid studies for the treatment of community-acquired pneumonia in adults", section on 'Empiric therapy for atypical bacteria'.)

Adverse effects — Both the macrolides and the fluoroquinolones can cause a prolonged QT interval, which can result in torsades de pointes and death. Studies assessing the risk-benefit ratio of azithromycin are reviewed elsewhere. Since the use of macrolides (and azithromycin in particular) has been associated with reduced mortality in CAP patients who require hospitalization, the risks and benefits should be considered when selecting a regimen. For the general population, azithromycin can be prescribed without significant concern; for patients at high risk of QT interval prolongation, the use of azithromycin should be weighed against the risk of cardiac effects. For patients with known QT interval prolongation, we favor doxycycline since it has not been associated with QT interval prolongation. However, doxycycline should be avoided during pregnancy. It should also be noted that doxycycline has been less well studied for the treatment of CAP than the macrolides and fluoroquinolones. Patients at particular risk for QT prolongation include those with existing QT interval prolongation, hypokalemia, hypomagnesemia, significant bradycardia, bradyarrhythmias, uncompensated heart failure, and those receiving certain antiarrhythmic drugs (eg, class IA [quinidine, procainamide] or class III [dofetilide, amiodarone, sotalol] antiarrhythmic drugs). Older adult patients may also be more susceptible to drug-associated QT interval prolongation. (See "Fluoroquinolones", section on 'QT interval prolongation and arrhythmia' and "Azithromycin, clarithromycin, and telithromycin", section on 'QT interval prolongation and cardiovascular events' and "Acquired long QT syndrome" and "Pharmacology of azoles", section on 'Selected clinical effects'.)

There is concern that widespread use of fluoroquinolones will promote the development of fluoroquinolone resistance among respiratory pathogens (as well as other colonizing pathogens) and, as noted above, increases the risk of C. difficile colitis. In addition, empiric use of fluoroquinolones should not be used for patients at risk for M. tuberculosis without an appropriate assessment for tuberculosis infection. The administration of a fluoroquinolone in patients with tuberculosis has been associated with a delay in diagnosis, increase in resistance, and poor outcomes. (See "Antibiotic and glucocorticoid studies for the treatment of community-acquired pneumonia in adults", section on 'Fluoroquinolone resistance' and "Clostridium difficile in adults: Epidemiology, microbiology, and pathophysiology", section on 'Antibiotic use'.)

Risk factors for rehospitalization — Risk factors for rehospitalization were assessed in a multicenter randomized trial of hospitalized patients with CAP [76]. Among 577 patients, 70 (12 percent) were rehospitalized within 30 days, 52 were related to comorbidities (most commonly cardiovascular, pulmonary, or neurologic), and 14 were related to pneumonia. Factors that were independently associated with rehospitalization included less than a high school education, unemployment, coronary artery disease, and chronic obstructive pulmonary disease.

In a similar study of 1117 patients from a single center, 81 (7 percent) were rehospitalized within 30 days; 29 due to pneumonia-related causes and the remainder due to pneumonia-unrelated causes [77]. Risk factors for pneumonia-related rehospitalization were initial treatment failure and one or more instability factors (eg, vital signs or oxygenation) on discharge; risk factors for non-pneumonia-related readmissions were age ≥65 and decompensated comorbidities (most commonly cardiac or pulmonary).

PREVENTIVE MEASURES

Vaccination — Patients with community-acquired pneumonia should be appropriately vaccinated for influenza and pneumococcal infection [2]. Screening for influenza vaccination status is warranted during influenza season (eg, from October through March in the northern hemisphere) in all patients. Screening for pneumococcal vaccination status is warranted in patients age 65 or older or with other indications for vaccination (table 8). Vaccination can be administered at any time during hospitalization after the patient has become stable. (See "Seasonal influenza vaccination in adults" and "Pneumococcal vaccination in adults".)

Smoking cessation — Smoking cessation should be a goal for hospitalized patients with community-acquired pneumonia who smoke [2]. (See "Overview of smoking cessation management in adults".)

Fall prevention — It is important to ensure that patients, particularly older patients, are mobilized early and often during their hospitalization to prevent falls and reduce functional decline. (See "Hospital management of older adults", section on 'Early mobilization programs'.)

GUIDELINES — A number of medical societies have issued guidelines for the treatment of community-acquired pneumonia (CAP) [2,78-80]. The antibiotic regimens advocated by a collaboration between the Infectious Diseases Society of America (IDSA)/American Thoracic Society (ATS) in 2007 [2] and the British Thoracic Society (BTS) in 2009 [78] are summarized in the tables (table 5 and table 9).

The recommendations in this topic are generally in keeping with the IDSA/ATS guidelines. Recommendations from these and other guidelines are summarized as follows:

For hospitalized patients on the general wards, the IDSA/ATS guidelines recommend an antipneumococcal fluoroquinolone (eg, levofloxacin, moxifloxacin, gemifloxacin) or the combination of a beta-lactam plus a macrolide (table 5) [2].

For patients with severe CAP requiring intensive care unit (ICU) admission, the IDSA/ATS guidelines recommend a beta-lactam (ceftriaxone, cefotaxime, ampicillin-sulbactam) plus either intravenous azithromycin or an antipneumococcal fluoroquinolone unless there is concern for Pseudomonas or methicillin-resistant S. aureus (MRSA) infection. If Pseudomonas is a concern, an antipseudomonal agent (piperacillin-tazobactam, imipenem, meropenem, or cefepime) PLUS an antipseudomonal fluoroquinolone (ciprofloxacin or high-dose levofloxacin) should be used. If MRSA is a concern, either vancomycin or linezolid should be added (table 5) [2]. (See 'Intensive care unit' above.)

The BTS and National Institute for Health and Care Excellence (NICE) guidelines tend to select older antibiotics than those recommended in North America (table 9) [78,81].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Community-acquired pneumonia in adults".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Community-acquired pneumonia in adults (The Basics)")

Beyond the Basics topics (see "Patient education: Pneumonia in adults (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Most initial treatment regimens for hospitalized patients with community-acquired pneumonia (CAP) are empiric. A limited number of pathogens are responsible for the majority of cases (table 1 and table 2 and figure 1) for which a pathogen is known, but in most cases a pathogen is not identified. The most commonly detected bacterial pathogen is Streptococcus pneumoniae. Other common pathogens include Haemophilus influenzae, the atypical bacteria (Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella spp), oropharyngeal aerobes and anaerobes (in the setting of aspiration), and respiratory viruses. Antibiotics should be started as soon as possible once the diagnosis of bacterial CAP is considered likely. (See 'Likely pathogens' above.)

The approach to diagnostic testing for hospitalized patients with CAP is summarized in the following table (table 3). In addition to the tests recommended in the table, we recommend testing for a specific organism when, based on clinical or epidemiologic data, pathogens that would not respond to usual empiric therapy are suspected (table 4). (See 'Diagnostic testing' above.)

For hospitalized patients not requiring intensive care unit (ICU) admission, we suggest initial combination therapy with an anti-pneumococcal beta-lactam (ceftriaxone, cefotaxime, ceftaroline, ertapenem, or ampicillin-sulbactam) plus a macrolide (azithromycin or clarithromycin XL) (algorithm 2) (Grade 2C).

For patients who cannot take a macrolide, we suggest monotherapy with a respiratory fluoroquinolone (levofloxacin, moxifloxacin, or gemifloxacin) (Grade 2C). Coverage for Pseudomonas or drug-resistant pathogens, such as MRSA, should be included in patients with risk factors. Doxycycline may be used as an alternative to a macrolide, especially in patients at high risk of QT interval prolongation. Oral therapy with a macrolide or doxycycline is appropriate only for selected patients without evidence of or risk factors for severe pneumonia. (See 'Medical ward' above.)

For hospitalized patients requiring ICU care, we suggest initial combination therapy with an anti-pneumococcal beta-lactam (ceftriaxone, cefotaxime, ceftaroline, or ampicillin-sulbactam) plus intravenous (IV) therapy with azithromycin (Grade 2C). For patients who cannot take azithromycin, we suggest a respiratory fluoroquinolone (levofloxacin or moxifloxacin) for the second agent (ie, in combination with a beta-lactam) (Grade 2C).

For patients with MRSA risk factors, we suggest the addition of either vancomycin (15 mg/kg IV every 12 hours, adjusted to a trough level of 15 to 20 mcg/mL and for renal function; in seriously ill patients, a loading dose of 25 to 30 mg/kg may be given) or linezolid (600 mg IV every 12 hours) (algorithm 3) (Grade 2B).

For patients at risk for Pseudomonas or drug-resistant pathogens, coverage for these pathogens should be included. (See 'Intensive care unit' above.)

For most patients with CAP who require intensive care unit admission, we recommend adjunctive glucocorticoids (Grade 1B). We are more likely to give glucocorticoids to more severely ill patients, especially those with a high systemic inflammatory response (C-reactive protein >15 mg/dL [>150 mg/L]), and we are less likely to give glucocorticoids to patients at increased risk of adverse effects. In patients at elevated risk of adverse effects, clinicians should make the decision about whether to give glucocorticoids on a case-by-case basis. When we give glucocorticoids to patients who are unable to take oral medications, we use methylprednisolone 0.5 mg/kg IV every 12 hours. For patients who can take oral medications, we use prednisone 50 mg orally daily. We continue glucocorticoids for a total of five days. There is limited evidence that infections caused by certain pathogens (eg, influenza virus, Aspergillus spp) may be associated with worse outcomes in the setting of glucocorticoid use; given these concerns, we avoid adjunctive glucocorticoids if one of these pathogens is detected. (See 'Adjunctive glucocorticoids' above.)

Once a pathogen has been established based upon reliable microbiologic methods, we favor narrowing therapy ("de-escalation") to target the specific pathogen in order to avoid antibiotic overuse. (See 'Narrowing therapy' above.)

Patients should be switched from intravenous to oral therapy when they are hemodynamically stable, demonstrate some clinical improvement (in fever, respiratory status, white blood count), and are able to take oral medications (algorithm 4). (See 'Switching to oral therapy' above.)

Hospital discharge is appropriate when the patient is clinically stable from the pneumonia, can take oral medication, has no other active medical problems, and has a safe environment for continued care; patients do not need to be kept overnight for observation following the switch. Patients who have been discharged from the hospital with CAP should have a follow-up visit, usually within one week. (See 'Duration of hospitalization' above and 'Clinical follow-up after discharge' above.)

Duration of treatment in patients with CAP who have a good clinical response within the first two to three days of therapy should generally be five to seven days. Longer treatment is indicated if the initial therapy was not active against the subsequently identified pathogen, if extrapulmonary infection is identified (eg, meningitis or endocarditis), or if the patient has documented P. aeruginosa, S. aureus, or Legionella pneumonia or pneumonia caused by some less common pathogens (algorithm 5). The duration of therapy in these patients should be individualized based upon the clinical response to treatment and patient comorbidities. For the treatment of MRSA pneumonia, we recommend a treatment duration of 7 to 21 days, depending upon the extent of infection and response to therapy; the shorter duration is recommended if the patient has a clear and early clinical response and no evidence of metastatic infection. (See 'Duration of therapy' above.)

Procalcitonin has been evaluated for guiding the decision to stop antibiotics since the procalcitonin level appears to correlate with the likelihood of a bacterial infection. We favor the use of procalcitonin to help guide the duration of therapy. (See 'Duration of therapy' above.)

Most patients with clinical resolution after treatment do not require a follow-up chest radiograph. We perform chest radiograph at 7 to 12 weeks following treatment in patients >50 years of age, particularly in males and smokers in this age group. (See 'Radiographic response' above.)

Use of UpToDate is subject to the  Subscription and License Agreement.

REFERENCES

  1. File TM. Community-acquired pneumonia. Lancet 2003; 362:1991.
  2. 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 2007; 44 Suppl 2:S27.
  3. Wunderink RG, Waterer GW. Clinical practice. Community-acquired pneumonia. N Engl J Med 2014; 370:543.
  4. Musher DM, Thorner AR. Community-acquired pneumonia. N Engl J Med 2014; 371:1619.
  5. Prina E, Ranzani OT, Torres A. Community-acquired pneumonia. Lancet 2015; 386:1097.
  6. Chalmers JD, Rother C, Salih W, Ewig S. Healthcare-associated pneumonia does not accurately identify potentially resistant pathogens: a systematic review and meta-analysis. Clin Infect Dis 2014; 58:330.
  7. Gross AE, Van Schooneveld TC, Olsen KM, et al. Epidemiology and predictors of multidrug-resistant community-acquired and health care-associated pneumonia. Antimicrob Agents Chemother 2014; 58:5262.
  8. Yap V, Datta D, Metersky ML. Is the present definition of health care-associated pneumonia the best way to define risk of infection with antibiotic-resistant pathogens? Infect Dis Clin North Am 2013; 27:1.
  9. Lopez A, Amaro R, Polverino E. Does health care associated pneumonia really exist? Eur J Intern Med 2012; 23:407.
  10. Attridge RT, Frei CR. Health care-associated pneumonia: an evidence-based review. Am J Med 2011; 124:689.
  11. Shorr AF, Zilberberg MD, Reichley R, et al. Validation of a clinical score for assessing the risk of resistant pathogens in patients with pneumonia presenting to the emergency department. Clin Infect Dis 2012; 54:193.
  12. Webb BJ, Dascomb K, Stenehjem E, et al. Derivation and Multicenter Validation of the Drug Resistance in Pneumonia Clinical Prediction Score. Antimicrob Agents Chemother 2016; 60:2652.
  13. File TM Jr, Niederman MS. Antimicrobial therapy of community-acquired pneumonia. Infect Dis Clin North Am 2004; 18:993.
  14. Arancibia F, Bauer TT, Ewig S, et al. Community-acquired pneumonia due to gram-negative bacteria and pseudomonas aeruginosa: incidence, risk, and prognosis. Arch Intern Med 2002; 162:1849.
  15. Shindo Y, Ito R, Kobayashi D, et al. Risk factors for drug-resistant pathogens in community-acquired and healthcare-associated pneumonia. Am J Respir Crit Care Med 2013; 188:985.
  16. Kuster SP, Rudnick W, Shigayeva A, et al. Previous antibiotic exposure and antimicrobial resistance in invasive pneumococcal disease: results from prospective surveillance. Clin Infect Dis 2014; 59:944.
  17. File TM Jr. New diagnostic tests for pneumonia: what is their role in clinical practice? Clin Chest Med 2011; 32:417.
  18. Read RC. Evidence-based medicine: empiric antibiotic therapy in community-acquired pneumonia. J Infect 1999; 39:171.
  19. Lode H, File TM Jr, Mandell L, et al. Oral gemifloxacin versus sequential therapy with intravenous ceftriaxone/oral cefuroxime with or without a macrolide in the treatment of patients hospitalized with community-acquired pneumonia: a randomized, open-label, multicenter study of clinical efficacy and tolerability. Clin Ther 2002; 24:1915.
  20. Lee JS, Giesler DL, Gellad WF, Fine MJ. Antibiotic Therapy for Adults Hospitalized With Community-Acquired Pneumonia: A Systematic Review. JAMA 2016; 315:593.
  21. Houck PM, Bratzler DW, Nsa W, et al. Timing of antibiotic administration and outcomes for Medicare patients hospitalized with community-acquired pneumonia. Arch Intern Med 2004; 164:637.
  22. Daniel P, Rodrigo C, Mckeever TM, et al. Time to first antibiotic and mortality in adults hospitalised with community-acquired pneumonia: a matched-propensity analysis. Thorax 2016; 71:568.
  23. Ruhe J, Mildvan D. Does empirical therapy with a fluoroquinolone or the combination of a β-lactam plus a macrolide result in better outcomes for patients admitted to the general ward? Infect Dis Clin North Am 2013; 27:115.
  24. US Food and Drug Administration (FDA). FDA drug safety communication: Increased risk of death with Tygacil (tigecycline) compared to other antibiotics used to treat similar infections. http://www.fda.gov/Drugs/DrugSafety/ucm224370.htm (Accessed September 2, 2010) (Accessed on September 02, 2010).
  25. Prasad P, Sun J, Danner RL, Natanson C. Excess deaths associated with tigecycline after approval based on noninferiority trials. Clin Infect Dis 2012; 54:1699.
  26. US Food and Drug Administration (FDA). FDA drug safety communication: FDA warns of increased risk of death with IV antibacterial Tygacil (tigecycline) and approves new boxed warning. http://www.fda.gov/Drugs/DrugSafety/ucm369580.htm (Accessed on October 09, 2013).
  27. Fiore AE, Fry A, Shay D, et al. Antiviral agents for the treatment and chemoprophylaxis of influenza --- recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep 2011; 60:1.
  28. Sibila O, Restrepo MI, Anzueto A. What is the best antimicrobial treatment for severe community-acquired pneumonia (including the role of steroids and statins and other immunomodulatory agents). Infect Dis Clin North Am 2013; 27:133.
  29. Restrepo MI, Anzueto A, Torres A. Corticosteroids for Severe Community-Acquired Pneumonia: Time to Change Clinical Practice. Ann Intern Med 2015; 163:560.
  30. Torres A, Ferrer M. What's new in severe community-acquired pneumonia? Corticosteroids as adjunctive treatment to antibiotics. Intensive Care Med 2016; 42:1276.
  31. Parody R, Martino R, Sánchez F, et al. Predicting survival in adults with invasive aspergillosis during therapy for hematological malignancies or after hematopoietic stem cell transplantation: Single-center analysis and validation of the Seattle, French, and Strasbourg prognostic indexes. Am J Hematol 2009; 84:571.
  32. Rodrigo C, Leonardi-Bee J, Nguyen-Van-Tam J, Lim WS. Corticosteroids as adjunctive therapy in the treatment of influenza. Cochrane Database Syst Rev 2016; 3:CD010406.
  33. Siemieniuk RA, Meade MO, Alonso-Coello P, et al. Corticosteroid Therapy for Patients Hospitalized With Community-Acquired Pneumonia: A Systematic Review and Meta-analysis. Ann Intern Med 2015; 163:519.
  34. Halm EA, Fine MJ, Marrie TJ, et al. Time to clinical stability in patients hospitalized with community-acquired pneumonia: implications for practice guidelines. JAMA 1998; 279:1452.
  35. Menéndez R, Torres A, Rodríguez de Castro F, et al. Reaching stability in community-acquired pneumonia: the effects of the severity of disease, treatment, and the characteristics of patients. Clin Infect Dis 2004; 39:1783.
  36. Fine MJ, Stone RA, Singer DE, et al. Processes and outcomes of care for patients with community-acquired pneumonia: results from the Pneumonia Patient Outcomes Research Team (PORT) cohort study. Arch Intern Med 1999; 159:970.
  37. Bruns AH, Oosterheert JJ, Prokop M, et al. Patterns of resolution of chest radiograph abnormalities in adults hospitalized with severe community-acquired pneumonia. Clin Infect Dis 2007; 45:983.
  38. Mittl RL Jr, Schwab RJ, Duchin JS, et al. Radiographic resolution of community-acquired pneumonia. Am J Respir Crit Care Med 1994; 149:630.
  39. El Solh AA, Aquilina AT, Gunen H, Ramadan F. Radiographic resolution of community-acquired bacterial pneumonia in the elderly. J Am Geriatr Soc 2004; 52:224.
  40. Almirall J, Bolíbar I, Vidal J, et al. Epidemiology of community-acquired pneumonia in adults: a population-based study. Eur Respir J 2000; 15:757.
  41. van der Eerden MM, Vlaspolder F, de Graaff CS, et al. Comparison between pathogen directed antibiotic treatment and empirical broad spectrum antibiotic treatment in patients with community acquired pneumonia: a prospective randomised study. Thorax 2005; 60:672.
  42. Ramirez JA, Srinath L, Ahkee S, et al. Early switch from intravenous to oral cephalosporins in the treatment of hospitalized patients with community-acquired pneumonia. Arch Intern Med 1995; 155:1273.
  43. Ramirez JA, Vargas S, Ritter GW, et al. Early switch from intravenous to oral antibiotics and early hospital discharge: a prospective observational study of 200 consecutive patients with community-acquired pneumonia. Arch Intern Med 1999; 159:2449.
  44. Oosterheert JJ, Bonten MJ, Schneider MM, et al. Effectiveness of early switch from intravenous to oral antibiotics in severe community acquired pneumonia: multicentre randomised trial. BMJ 2006; 333:1193.
  45. Carratalà J, Garcia-Vidal C, Ortega L, et al. Effect of a 3-step critical pathway to reduce duration of intravenous antibiotic therapy and length of stay in community-acquired pneumonia: a randomized controlled trial. Arch Intern Med 2012; 172:922.
  46. Ramirez JA, Bordon J. Early switch from intravenous to oral antibiotics in hospitalized patients with bacteremic community-acquired Streptococcus pneumoniae pneumonia. Arch Intern Med 2001; 161:848.
  47. Dunn AS, Peterson KL, Schechter CB, et al. The utility of an in-hospital observation period after discontinuing intravenous antibiotics. Am J Med 1999; 106:6.
  48. Nathan RV, Rhew DC, Murray C, et al. In-hospital observation after antibiotic switch in pneumonia: a national evaluation. Am J Med 2006; 119:512.e1.
  49. Dagan E, Novack V, Porath A. Adverse outcomes in patients with community acquired pneumonia discharged with clinical instability from Internal Medicine Department. Scand J Infect Dis 2006; 38:860.
  50. Hayashi Y, Paterson DL. Strategies for reduction in duration of antibiotic use in hospitalized patients. Clin Infect Dis 2011; 52:1232.
  51. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis 2011; 52:e18.
  52. Combes A, Luyt CE, Fagon JY, et al. Impact of methicillin resistance on outcome of Staphylococcus aureus ventilator-associated pneumonia. Am J Respir Crit Care Med 2004; 170:786.
  53. Avdic E, Cushinotto LA, Hughes AH, et al. Impact of an antimicrobial stewardship intervention on shortening the duration of therapy for community-acquired pneumonia. Clin Infect Dis 2012; 54:1581.
  54. Mitsuma SF, Mansour MK, Dekker JP, et al. Promising new assays and technologies for the diagnosis and management of infectious diseases. Clin Infect Dis 2013; 56:996.
  55. Schuetz P, Müller B, Christ-Crain M, et al. Procalcitonin to initiate or discontinue antibiotics in acute respiratory tract infections. Cochrane Database Syst Rev 2012; :CD007498.
  56. Bartlett JG, Dowell SF, Mandell LA, et al. Practice guidelines for the management of community-acquired pneumonia in adults. Infectious Diseases Society of America. Clin Infect Dis 2000; 31:347.
  57. Tang KL, Eurich DT, Minhas-Sandhu JK, et al. Incidence, correlates, and chest radiographic yield of new lung cancer diagnosis in 3398 patients with pneumonia. Arch Intern Med 2011; 171:1193.
  58. Wunderink RG, Niederman MS, Kollef MH, et al. Linezolid in methicillin-resistant Staphylococcus aureus nosocomial pneumonia: a randomized, controlled study. Clin Infect Dis 2012; 54:621.
  59. Kalil AC, Klompas M, Haynatzki G, Rupp ME. Treatment of hospital-acquired pneumonia with linezolid or vancomycin: a systematic review and meta-analysis. BMJ Open 2013; 3:e003912.
  60. Rubinstein E, Kollef MH, Nathwani D. Pneumonia caused by methicillin-resistant Staphylococcus aureus. Clin Infect Dis 2008; 46 Suppl 5:S378.
  61. Hageman JC, Uyeki TM, Francis JS, et al. Severe community-acquired pneumonia due to Staphylococcus aureus, 2003-04 influenza season. Emerg Infect Dis 2006; 12:894.
  62. Francis JS, Doherty MC, Lopatin U, et al. Severe community-onset pneumonia in healthy adults caused by methicillin-resistant Staphylococcus aureus carrying the Panton-Valentine leukocidin genes. Clin Infect Dis 2005; 40:100.
  63. Labandeira-Rey M, Couzon F, Boisset S, et al. Staphylococcus aureus Panton-Valentine leukocidin causes necrotizing pneumonia. Science 2007; 315:1130.
  64. Gillet Y, Issartel B, Vanhems P, et al. Association between Staphylococcus aureus strains carrying gene for Panton-Valentine leukocidin and highly lethal necrotising pneumonia in young immunocompetent patients. Lancet 2002; 359:753.
  65. Graves SF, Kobayashi SD, Braughton KR, et al. Relative contribution of Panton-Valentine leukocidin to PMN plasma membrane permeability and lysis caused by USA300 and USA400 culture supernatants. Microbes Infect 2010; 12:446.
  66. Li M, Diep BA, Villaruz AE, et al. Evolution of virulence in epidemic community-associated methicillin-resistant Staphylococcus aureus. Proc Natl Acad Sci U S A 2009; 106:5883.
  67. Diep BA, Chan L, Tattevin P, et al. Polymorphonuclear leukocytes mediate Staphylococcus aureus Panton-Valentine leukocidin-induced lung inflammation and injury. Proc Natl Acad Sci U S A 2010; 107:5587.
  68. Bubeck Wardenburg J, Palazzolo-Ballance AM, Otto M, et al. Panton-Valentine leukocidin is not a virulence determinant in murine models of community-associated methicillin-resistant Staphylococcus aureus disease. J Infect Dis 2008; 198:1166.
  69. Peyrani P, Allen M, Wiemken TL, et al. Severity of disease and clinical outcomes in patients with hospital-acquired pneumonia due to methicillin-resistant Staphylococcus aureus strains not influenced by the presence of the Panton-Valentine leukocidin gene. Clin Infect Dis 2011; 53:766.
  70. Bernardo K, Pakulat N, Fleer S, et al. Subinhibitory concentrations of linezolid reduce Staphylococcus aureus virulence factor expression. Antimicrob Agents Chemother 2004; 48:546.
  71. Stevens DL, Ma Y, Salmi DB, et al. Impact of antibiotics on expression of virulence-associated exotoxin genes in methicillin-sensitive and methicillin-resistant Staphylococcus aureus. J Infect Dis 2007; 195:202.
  72. Vesga O, Agudelo M, Salazar BE, et al. Generic vancomycin products fail in vivo despite being pharmaceutical equivalents of the innovator. Antimicrob Agents Chemother 2010; 54:3271.
  73. Kallen AJ, Brunkard J, Moore Z, et al. Staphylococcus aureus community-acquired pneumonia during the 2006 to 2007 influenza season. Ann Emerg Med 2009; 53:358.
  74. File TM Jr, Marrie TJ. Does empiric therapy for atypical pathogens improve outcomes for patients with CAP? Infect Dis Clin North Am 2013; 27:99.
  75. File TM Jr, Eckburg PB, Talbot GH, et al. Macrolide therapy for community-acquired pneumonia due to atypical pathogens: outcome assessment at an early time point. Int J Antimicrob Agents 2017; 50:247.
  76. Jasti H, Mortensen EM, Obrosky DS, et al. Causes and risk factors for rehospitalization of patients hospitalized with community-acquired pneumonia. Clin Infect Dis 2008; 46:550.
  77. Capelastegui A, España Yandiola PP, Quintana JM, et al. Predictors of short-term rehospitalization following discharge of patients hospitalized with community-acquired pneumonia. Chest 2009; 136:1079.
  78. Lim WS, Baudouin SV, George RC, et al. BTS guidelines for the management of community acquired pneumonia in adults: update 2009. Thorax 2009; 64 Suppl 3:iii1.
  79. Mandell LA, Marrie TJ, Grossman RF, et al. Canadian guidelines for the initial management of community-acquired pneumonia: an evidence-based update by the Canadian Infectious Diseases Society and the Canadian Thoracic Society. The Canadian Community-Acquired Pneumonia Working Group. Clin Infect Dis 2000; 31:383.
  80. Johnstone J, Mandell L. Guidelines and quality measures: do they improve outcomes of patients with community-acquired pneumonia? Infect Dis Clin North Am 2013; 27:71.
  81. National Institute for Health and Care Excellence. Pneumonia: Diagnosis and management of community- and hospital-acquired pneumonia in adults. NICE guidelines, 2014. https://www.nice.org. uk/guidance (Accessed on February 14, 2016).
Topic 7027 Version 83.0

Topic Outline

GRAPHICS

RELATED TOPICS

All topics are updated as new information becomes available. Our peer review process typically takes one to six weeks depending on the issue.