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Treatment of Community-Acquired Pneumonia: A Case Report and Current Treatment Dilemmas

Glenn harnett.

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*Glenn Harnett: [email protected]

Academic Editor: Ching H. Loh

Received 2016 Dec 16; Accepted 2017 Apr 13; Issue date 2017.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Resistance to macrolides is rising in the USA and warrants careful consideration when confronted with a patient with suspected pneumonia in the urgent care clinic. This case study exemplifies the potentially serious consequences of treatment failure following prescription of a macrolide for community-acquired bacterial pneumonia. Furthermore, the consequential treatment dilemmas currently faced by physicians are briefly discussed.

1. Introduction

Each year, over 4 million ambulatory patients are treated for community-acquired pneumonia (CAP) in the United States (US) [ 1 ], with approximately 80% treated on an outpatient basis [ 2 ]. Community-acquired bacterial pneumonia (CABP) is a common presenting illness in the urgent care setting, yet many providers underappreciate the mortality associated with pneumonia and underrate how commonly it occurs—CABP is in fact the leading cause of infectious death in adults and the number of deaths is higher than either breast or prostate cancer [ 3 ].

This case report describes common historical and physical examination findings in CABP and the use of traditional and more modern diagnostic tools, as well as treatment dilemmas currently facing clinicians.

Streptococcus pneumoniae remains the leading bacterial cause of pneumonia in the United States and globally. Moreover, of particular concern to public health agencies and clinicians is that S. pneumoniae is rapidly becoming more resistant to currently available antibiotics, elevating to prominence new phenotype serotypes referred to as drug-resistant S. pneumoniae (DRSP).

These DRSP serotypes are particularly resistant to currently available macrolides, such as azithromycin. S. pneumoniae macrolide resistance rates are as high as 60% or more in some regions of the US [ 1 ]. The current IDSA/ATS guidelines on the management of CAP (soon to be updated) recommend the use of an alternative to macrolides in areas where “high-level” (minimum inhibitory concentration [MIC] ≥ 16  µ g/mL) macrolide-resistant S. pneumoniae rates are greater than 25% [ 4 ]. Keep in mind that presently those areas include the entire US, other than the CDC defined mountain region [ 5 ]. Despite this, macrolides are used to treat approximately 40% of CABP cases in the US [ 6 ].

Clinicians should also be aware of the correlation between pneumonia and influenza. Influenza is a predisposing factor for acquiring pneumonia, especially in older adults and those with comorbid conditions (see later). Indeed, pneumonia is the most common significant complication of influenza and leads to significant morbidity and mortality.

2. Case Presentation

A 66-year-old male presented to an urgent care clinic with a 4-day history of dry cough, progressing to rusty colored sputum, sudden onset of chills the previous evening, subjective fever, and malaise. Originally, the man thought he had a cold, but the symptoms had worsened and he “barely slept last night with all this coughing.”

He denied experiencing shortness of breath but suggested he may be breathing “a little faster than normal.” He related that, on the way to the clinic, he felt some sharp right-sided chest pain after a particularly long bout of coughing. He denied any leg swelling, orthopnea, or left-sided/substernal chest pain. He also denied any gastrointestinal symptoms (no nausea, vomiting, or diarrhea). His past medical history included hypertension and hypercholesterolemia. He reported no antibiotic use in the previous three months.

He was anxious to “get something to clear this up” as he had plans to attend his first granddaughter's destination-wedding in the Caribbean in one week's time.

3. Physical Examination

In general, the man appeared tired and a bit “washed out.” His vital signs were as follows:

Temperature (F): 101.3

Blood pressure (mmHg): 128/76

HR (bpm): 102

RR (bpm): 24

SpO 2 (%): 94

Respiratory examination revealed mild tachypnea with dullness to percussion over the lower-right lung. Auscultation revealed decreased breath sounds in the same area, but no crackles or wheezing.

Other than mild tachycardia with a regular rhythm, the remainder of the physical examination was normal. There was no jugular venous distention or pedal edema. For comparison and consideration, other theoretical physical examination findings that would have been indicative of pneumonia are presented in Table 1 [ 7 ], and the differential diagnosis is in Table 2 .

Physical examination findings in CAP [ 7 ].

a may indicate Legionella etiology; b may indicate an anaerobic and/or polymicrobial infection; c may indicate a Mycoplasma pneumonia infection; d may indicate a Nocardia infection via hematogenous spread from a pulmonary focus.

Differential diagnosis in CAP.

MI, myocardial infarction; RSV, respiratory syncytial virus; COPD, chronic obstructive pulmonary disease; PCP, Pneumocystis jirovecii pneumonia.

4. Diagnostic Results

The “gold standard” for diagnosis of CABP is the chest X-ray. When pneumonia is suspected based on history of present illness, subjective symptoms, and physical exam, the clinician should obtain a standard chest radiograph with PA and lateral views. The chest X-ray can also be helpful in “ruling out” other potential causes of symptoms, even if infiltrates may not always be visible to confirm CABP with some early presentations of CABP. The man's chest X-ray revealed a lower-right lobar-type pneumonia without an effusion ( Figure 1 ).

Example of lower-right lobar shadow (red arrow) from a representative PA radiograph.

Table 3 shows selected results from the man's complete blood-cell count (CBC) and complete metabolic panel (CMP). Note that the patient's WBC (4,200 cells/uL) and percentage of lymphocytes (12%) was lower than normal (18–40%).

Selected patient CBC and CMP results.

AlkP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; CBC, complete blood-cell count; CMP, complete metabolic panel; BUN, blood urea nitrogen; WBC, white blood cell.

Although not done prior to initiating treatment in this case, other testing options may have included blood cultures, urine antigen testing for S. pneumoniae and Legionella, and sputum cultures. The vast majority of urgent care centers do not have the capability of performing blood cultures or collecting sputum samples, nor do many, at this point, routinely collect urine antigen samples in patients with presumed pneumonia.

5. Discussion

5.1. risk stratification.

Initial risk stratification in CABP helps guide diagnosis, treatment decisions, and patient disposition. Hospital admission is an important economic consideration in CABP as the cost of inpatient care for pneumonia is logarithmically higher than outpatient care (e.g., circa $27k versus $2k per episode, resp.) [ 9 , 10 ].

Moreover, low risk CABP patients ought to be treated as outpatients whenever possible to avoid complications of hospital-acquired superinfections and thromboembolic events [ 11 ]. CABP patients treated on an outpatient basis are also more likely to return to work and other activities faster than those admitted, while most patients prefer to be treated as an outpatient [ 12 ].

Providers making site-of-care treatment decisions need to consider barriers to outpatient treatment, such as frailty, lack of response to previous therapy, severe social or psychiatric problems, substance abuse, homelessness, and unstable living conditions.

Prognostic models, such as the PORT score (based on the Pneumonia Severity Index [PSI] scoring system), or severity-of-illness scores, such as the CURB-65 criteria, can aid the decision for outpatient treatment [ 4 ].

The CURB-65 scale is a simple way to determine pneumonia severity. Using CURB-65, providers assign 1 point for each criterion met in Figure 2 . If the individual scores 1 point or less, outpatient treatment is appropriate; 2 points indicate hospitalization and inpatient treatment. Greater than or equal to 3 points warrant inpatient treatment in the ICU [ 13 ]. In our patient's case, the CURB-65 score was 1, with the one point assigned based on his age of 66. He met none of the other CURB-65 criteria.

CURB-65 scoring: a simple, fast, and effective clinical decision tool for determining point of care setting in CAP. Urea/blood urea nitrogen (BUN) score can be excluded when unavailable in the urgent care setting. Figure adapted by authors from Lim et al., 2003, with permission [ 13 ]. ∗ Defined as a Mental Test Score of 8 or less or new disorientation in person, place, or time.

The use of the CURB-65 and PORT scores can be problematic in the urgent care setting as many centers do not have point of care chemistry testing and very few have access to arterial blood gas testing. However, even when tests are unavailable, the score for BUN can be excluded and if the patient still has a remaining CURB-65 score of 2 or higher, they clearly meet hospital admission criteria [ 13 ].

5.2. Pneumonia and Influenza

CABP together with influenza remains the 8th leading cause of death in the United States [ 14 ]. Between 1979 and 2009 there were an average of 66,000 deaths per year attributable to coinfection with influenza and pneumonia [ 3 ], with 55,227 deaths occurring in 2014 [ 14 ]. S. pneumoniae is the leading cause of pneumonia in those coinfected with influenza and leads to higher morbidity and mortality. A common mistaken perception is that influenza itself has a high mortality rate. Complications account for the majority of morbidity/mortality in influenza, with pneumonia being the leading significant complication [ 15 ].

Historical review of the 1918-19 influenza pandemic suggests that the majority of deaths were not a direct effect of the influenza virus but instead resulted from bacterial coinfection causing pneumonia [ 15 ]. This remains true today [ 17 ], and for that reason, clinicians treating patients with influenza need to have a high clinical suspicion for pneumonia.

In patients with influenza, coinfection with bacterial pneumonia is something clinicians cannot afford to miss. Risk factors for bacterial pneumonia coinfection in influenza are listed in Table 4 [ 8 ]. Other influenza complications may include bacteremia, sepsis, empyema, pericarditis, respiratory failure, and death.

Influenza patients at greater risk of bacterial pneumonia [ 8 ].

5.3. Treatment Options and Macrolide Resistance

The 2007 IDSA/ATS guidelines [ 4 ] recommend the antibiotic therapy options distilled in Table 5 for treatment of CAP. Guideline adherence and appropriate use of macrolides have been associated with reduced mortality in outpatients with pneumonia [ 18 ].

Summary ∗ of 2007 IDSA/ATS guidelines for outpatient treatment of community-acquired pneumonia [ 4 ].

∗ This distillation of recommendation is not intended to replace the guidelines, which contain details not shown here; DRSP, drug-resistant S. pneumoniae .

The guidelines provide detail not shown in Table 5 , such as weighting of recommendations based on level of evidence, definitions, and examples of terms [ 4 ].

Approximately 40% of S. Pneumoniae isolates in the US display in vitro resistance to macrolide antibiotics. This resistance has developed via 2 separate mechanisms:

Mef(A)-mediated resistance involves an efflux pump, resulting in low-level resistance. High local concentrations of macrolide antibiotics can overcome this type of resistance mechanism, resulting in good clinical efficacy despite in vitro resistance.

Erm(B)-mediated resistance involves a conformational change to the macrolide binding site at the bacterial 23S ribosomal subunit. This change confers high-level macrolide resistance.

Two-thirds of macrolide resistance in the US is related to the mef(A) mechanism. However, erm(B)-mediated “high-level” resistance appears to be increasing, with the potential to lead to increased clinical treatment failures for patients treated with macrolide monotherapy [ 19 ].

Important . In regions with “high-level” (minimum inhibitory concentration [MIC] ≥ 16  µ g/mL) macrolide-resistant S. pneumoniae , consider the use of nonmacrolide alternative agents listed in Table 2 , including those for patients without comorbidities [ 4 ]. Once again, keep in mind that only the mountain region of the USA has S. pneumoniae “high-level” (MIC ≥ 16 ug/ml) macrolide resistance rates lower than 25% ( Figure 3 ), which means that most clinicians should reconsider the use of macrolides as monotherapy in CAP.

Rate of macrolide-resistant S. pneumonia in 2014. Figure adapted by authors from Blondeau and Theriault, 2017 [ 16 ].

Along with local resistance rates, antibiotic selection should consider the patient's risk factors for possible infection with DRSP [ 5 , 16 , 20 ], including the following:

Recent antibiotic use (within 3 months)

Age greater than 65 years

Immunosuppressive illness

Multiple medical comorbidities

Exposure to a child attending a daycare center

Alcohol abuse

Asthma/COPD

Diabetes mellitus

Recent travel [ 5 ]

In the first decade of this millennium, DRSP risk factors were present in approximately half of outpatient CAP cases treated in the acute care setting. Despite this fact, physician adherence to guideline-concordant antibiotic therapy remained infrequent as clinicians continued to use macrolides, especially azithromycin, as CAP monotherapy [ 18 ]. This is despite the fact that guideline adherence and appropriate use of macrolides had been associated with reduced mortality in outpatients with pneumonia [ 18 ].

Remember that the most prevalent causative organism in CAP is S. pneumoniae , regardless of the host or setting. Empiric antibiotic therapy should always be selected with this microorganism in mind. The IDSA guidelines clearly recommend knowing the prevalence of high-level drug-resistant pneumococci in your geographic location to aid decision-making. Unfortunately, antibiograms are becoming less available to community physicians working outside the hospital setting. Healthcare leaders will need to work together to make these useful tools more available to clinicians as antibiotic resistant E. coli , S. aureus , and S. pneumoniae strains increasingly affect our patient population.

Response to antibiotic therapy for CABP should be evaluated within 48–72 hours of initiation of treatment. However, antibiotics should not be changed within the first 72 hours unless marked clinical deterioration occurs or the causative pathogen is identified. Chest X-rays usually clear within 4 weeks in patients younger than 50 years, but resolution may be delayed for 12 weeks or longer in older individuals. The benefit of routine radiography after pneumonia remains unclear. The most recent US guidelines do not address this issue, while a recent UK guideline recommends follow-up X-rays only for patients with persistent symptoms or those “at higher risk of underlying malignancy (especially smokers and those aged > 50 years)” [ 21 ].

6. Case Presentation: Patient Treatment Course and Outcome

Based on the patient's presentation and testing results, the patient was correctly diagnosed with CABP. Applying the CURB-65 criteria with a resultant score of 1, the man was appropriately treated on an outpatient basis. However, unaware that “high-level” S. pneumoniae macrolide resistance rates in the East South Central area are 48%, the provider placed the man on a “Z-PAK” (azithromycin) as CAP monotherapy.

Two days later, the man presented to the local ER with worsening symptoms that had progressed to include dyspnea and an oxygen saturation of 89%. He was admitted to the hospital for 5 days of inpatient treatment, including IV levofloxacin, with 2 days spent in the ICU. The patient did not require ventilator support. Blood cultures revealed S. pneumoniae resistant to azithromycin but sensitive to fluoroquinolones. The man survived his hospitalization.

Would further testing have changed the treatment plan or point of care decision? Blood cultures in CAP can be of questionable utility and are not routinely ordered in the outpatient setting. Obtaining blood cultures for non-ICU CAP patients is no longer core measure per CMS and JCAHO as of January 1, 2014. This is likely due to the fact that rates of positive blood cultures in confirmed CAP are only in the 8–15% range [ 20 , 22 ]. Positive rates are even lower in those with low risk CAP. Even in pneumococcal pneumonia, the results are often negative (although their yield may be higher in patients with more severe pneumonia/infection) [ 23 ].

Per IDSA/ATS Consensus Guidelines, S. pneumoniae urine antigen testing (UAT) is suggested if testing results will change the antibiotic management for patients with CAP. S. pneumoniae UAT is an option currently available in labs that are certified as COLA/CLIA moderately complex. IDSA clinical indications for S. pneumoniae UAT testing in outpatients (which ought to be reimbursed) include [ 4 ] the following:

Failure of outpatient antibiotic therapy

Active alcohol abuse

Severe liver disease

Pleural effusion

ICU admission

The man's CBC revealed that he was leukopenic and thereby met IDSA criteria for S. pneumoniae UAT testing. Considering the local antibiotic resistance rates, would a positive S. pneumoniae UAT test have changed the treatment plan in the man's case?

7. Considerations

Current IDSA/ATS guidelines recommend that in regions with a high rate (25%) of infection with high-level (MIC, ≥16 mg/mL) macrolide-resistant S. pneumoniae , macrolide monotherapy should be avoided [ 4 , 24 ]. In the USA, S. pneumoniae resistance rates are increasing across antibiotic class [ 25 ], with S. pneumoniae even being fully resistant to one or more antibiotics in 30% of severe pneumonia cases [ 26 ]. High-level macrolide resistance to S. pneumoniae is increasing [ 26 , 27 ], with many US states showing overall resistant rates greater than 40% ( Figure 3 ) [ 16 , 26 ].

Using the currently available macrolides as monotherapy in CABP should be reconsidered in this era of increased DSRP. Recently, Mandell suggested the increasing pneumococcal resistance to macrolides may diminish the use of these drugs as monotherapy for CAP [ 28 ]. Per the IDSA guidelines respiratory fluoroquinolones and doxycycline are the only other treatment considerations for monotherapy in CAP. A question that remains is how often high-level antibiotic resistance translates into actual treatment failure. Mandell points out that retrospective data show a positive correlation among macrolide resistance rates ≥ 25%, treatment failure, and costs [ 24 ]. Increased mortality in cases of CABP failing initial outpatient macrolide therapy was reported even with low-level macrolide resistance [ 29 ]. Other risks, besides treatment failure with macrolide monotherapy, includes the well documented “black box” side effects of the fluoroquinolones, such as tendinopathy, and their propensity for causing C. difficile enterocolitis [ 24 ]. Many infectious disease physicians worry that the fluoroquinolones are too broad spectrum for routine use in low risk outpatient treatment for CAP and that their use as monotherapy could lead to increased resistance in the future. Increasing antibiotic resistance rates to doxycycline have also limited its effectiveness as monotherapy in CAP [ 24 ].

This case illustrates the challenging outpatient treatment environment in which CABP resistance patterns have changed while our current arsenal of antibiotics has remained the same. Current awareness of resistance patterns is not ideal and providers need better access to local/regional information (antibiograms) and further education on preferred treatment options for CABP. New community-acquired pneumonia guidelines from the IDSA/ATS are expected in 2017. New antibiotics for the treatment of CAP are needed and hopes are that new regulatory processes such as those contained in Generating Antibiotic Incentives Now (GAIN) Act of 2012 will stimulate further antibiotic development. Another noteworthy CAP-related case you are encouraged to read was published by Aguilar et al., 2016 [ 30 ].

Acknowledgments

Dr. David Macari and Dr. Samantha Scott, representing Innovative Strategic Communications, LLC (Milford, PA, USA), provided assistance in preparing and editing the manuscript. Funding for this support was provided by Cempra Pharmaceuticals Inc. (Chapel Hill, NC, USA).

Conflicts of Interest

Dr. Glenn Harnett reports nonfinancial support (in the form of manuscript preparation and editorial assistance) from Innovative Strategic Communications, LLC (Milford, PA, USA), a medical communications agency funded by Cempra Pharmaceuticals Inc. (Chapel Hill, NC, USA). In addition, Dr. Harnett is a former member of the Speakers Bureau for Solithromycin, organized by Cempra Pharmaceuticals Inc. and Alere Inc. (Waltham, MA, USA) outside the submitted work.

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INTRODUCTION  — 

Community-acquired pneumonia (CAP) is a leading cause of morbidity and mortality worldwide. The clinical presentation of CAP varies, ranging from mild pneumonia characterized by fever and productive cough to severe pneumonia characterized by respiratory distress and sepsis. Because of the wide spectrum of associated clinical features, CAP is a part of the differential diagnosis of nearly all respiratory illnesses.

This topic provides a broad overview of the epidemiology, microbiology, pathogenesis, clinical features, diagnosis, and management of CAP in immunocompetent adults. Detailed discussions of each of these issues are presented separately; links to these discussions are provided within the text below.

DEFINITIONS  — 

Pneumonia is frequently categorized based on site of acquisition ( table 1 ).

● Community-acquired pneumonia (CAP) refers to an acute infection of the pulmonary parenchyma acquired outside of the hospital.

● Nosocomial pneumonia refers to an acute infection of the pulmonary parenchyma acquired in hospital settings and encompasses both hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP).

• HAP refers to pneumonia acquired ≥48 hours after hospital admission.

• VAP refers to pneumonia acquired ≥48 hours after endotracheal intubation.

Health care-associated pneumonia (HCAP; no longer used) referred to pneumonia acquired in health care facilities (eg, nursing homes, hemodialysis centers) or after recent hospitalization. The term HCAP was used to identify patients at risk for infection with multidrug-resistant pathogens. However, this categorization may have been overly sensitive, leading to increased, inappropriately broad antibiotic use and was thus retired. In general, patients previously classified as having HCAP should be treated similarly to those with CAP. (See "Epidemiology, pathogenesis, microbiology, and diagnosis of hospital-acquired and ventilator-associated pneumonia in adults" .)

EPIDEMIOLOGY

Incidence  —  CAP is one of the most common and morbid conditions encountered in clinical practice [ 1-3 ]. In the United States, CAP accounts for over 4.5 million outpatient and emergency room visits annually, corresponding to approximately 0.4 percent of all encounters [ 4 ]. CAP is the second most common cause of hospitalization and the most common infectious cause of death [ 5,6 ]. Approximately 650 adults are hospitalized with CAP every year per 100,000 population in the United States, corresponding to 1.5 million unique CAP hospitalizations each year [ 7 ]. Nearly 9 percent of patients hospitalized with CAP will be rehospitalized due to a new episode of CAP during the same year.

Risk factors

● Older age – The risk of CAP rises with age [ 7,8 ]. The annual incidence of hospitalization for CAP among adults ≥65 years old is approximately 2000 per 100,000 in the United States [ 7,9 ]. This figure is approximately three times higher than the general population and indicates that 2 percent of the older adult population will be hospitalized for CAP annually ( figure 1 ).

● Chronic comorbidities – The comorbidity that places patients at highest risk for CAP hospitalization is chronic obstructive pulmonary disease (COPD), with an annual incidence of 5832 per 100,000 in the United States [ 7 ]. Other comorbidities associated with an increased incidence of CAP include other forms of chronic lung disease (eg, bronchiectasis, asthma), chronic heart disease (particularly congestive heart failure), stroke, diabetes mellitus, malnutrition, and immunocompromising conditions ( figure 2 ) [ 7,10,11 ].

● Viral respiratory tract infection – Viral respiratory tract infections can lead to primary viral pneumonias and also predispose to secondary bacterial pneumonia. This is most pronounced for influenza virus infection. (See "Seasonal influenza in adults: Clinical manifestations and diagnosis", section on 'Pneumonia' .)

● Impaired airway protection – Conditions that increase risk of macroaspiration of stomach contents and/or microaspiration of upper airway secretions predispose to CAP, such as alteration in consciousness (eg, due to stroke, seizure, anesthesia, drug or alcohol use) or dysphagia due to esophageal lesions or dysmotility.

● Smoking and alcohol overuse – Smoking, alcohol overuse (eg, >80 g/day), and opioid use are key modifiable behavioral risk factors for CAP [ 7,10,12,13 ].

● Other lifestyle factors – Other factors that have been associated with an increased risk of CAP include crowded living conditions (eg, prisons, homeless shelters), residence in low-income settings, and exposure to environmental toxins (eg, solvents, paints, or gasoline) [ 7,10,11,14 ].

Combinations of risk factors, such as smoking, COPD, and congestive heart failure, are additive in terms of risk [ 15 ]. These risk factors and other predisposing conditions for the development of CAP are discussed separately. (See "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults", section on 'Predisposing host conditions' .)

MICROBIOLOGY

Common causes  —  Streptococcus pneumoniae (pneumococcus) and respiratory viruses are the most frequently detected pathogens in patients with CAP [ 8,16 ]. However, in a large proportion of cases (up to 62 percent in some studies performed in hospital settings), no pathogen is detected despite extensive microbiologic evaluation [ 8,17,18 ].

The most commonly identified causes of CAP can be grouped into three categories:

● Typical bacteria

• S. pneumoniae (most common bacterial cause)

• Haemophilus influenzae

• Moraxella catarrhalis

• Staphylococcus aureus

• Group A streptococci

• Aerobic gram-negative bacteria (eg, Enterobacteriaceae such as Klebsiella spp or Escherichia coli )

• Microaerophilic bacteria and anaerobes (associated with aspiration)

● Atypical bacteria ("atypical" refers to the intrinsic resistance of these organisms to beta-lactams and their inability to be visualized on Gram stain or cultured using traditional techniques)

• Legionella spp

• Mycoplasma pneumoniae

• Chlamydia pneumoniae

• Chlamydia psittaci

• Coxiella burnetii

● Respiratory viruses

• Influenza A and B viruses

• Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)

• Other coronaviruses (eg, CoV-229E, CoV-NL63, CoV-OC43, CoV-HKU1)

• Rhinoviruses

• Parainfluenza viruses

• Adenoviruses

• Respiratory syncytial virus

• Human metapneumovirus

• Human bocaviruses

The relative prevalence of these pathogens varies with geography, pneumococcal vaccination rates, host risk factors (eg, smoking), season, and pneumonia severity ( table 2 ).

Certain epidemiologic exposures also raise the likelihood of infection with a particular pathogen ( table 3 ). As examples, exposure to contaminated water is a risk factor for Legionella infection, exposure to birds raises the possibility of C. psittaci infection, travel or residence in the southwestern United States should raise suspicion for coccidioidomycosis, and poor dental hygiene may predispose patients with pneumonia caused by oral flora or anaerobes. In immunocompromised patients, the spectrum of possible pathogens also broadens to include fungi and parasites as well as less common bacterial and viral pathogens. (See "Epidemiology of pulmonary infections in immunocompromised patients" and "Approach to the immunocompromised patient with fever and pulmonary infiltrates" .)

While the list above details some of most common causes of CAP, >100 bacterial, viral, fungal, and parasitic causes have been reported. (See "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults", section on 'Microbiology' .)

Important trends  —  Both the distribution of pathogens that cause CAP and our knowledge of these pathogens are evolving. Key observations that have changed our understanding of CAP and influenced our approach to management include:

● Decline in S. pneumoniae incidence – Although S. pneumoniae (pneumococcus) is the most commonly detected bacterial cause of CAP in most studies, the overall incidence of pneumococcal pneumonia is decreasing. This is in part due to widespread use of pneumococcal vaccination, which results in both a decline in the individual rates of pneumococcal pneumonia and herd immunity in the population. (See "Pneumococcal pneumonia in patients requiring hospitalization", section on 'Prevalence' .)

Because pneumococcal vaccination rates vary regionally, the prevalence of S. pneumoniae infection also varies. As an example, S. pneumoniae is estimated to cause approximately 30 percent of cases of CAP in Europe but only 10 to 15 percent in the United States, where the population pneumococcal vaccination rate is higher [ 8 ].

● The coronavirus disease 2019 (COVID-19) pandemic – SARS-CoV-2 is an important cause of CAP and is discussed in detail elsewhere. (See "COVID-19: Epidemiology, virology, and prevention" .)

● Increased recognition of other respiratory viruses – Respiratory viruses have been detected in approximately one-third of cases of CAP in adults when using molecular methods [ 8 ]. The extent to which respiratory viruses serve as single pathogens, cofactors in the development of bacterial CAP, or triggers for dysregulated host immune response has not been established.

● Low overall rate of pathogen detection – Despite extensive evaluation using molecular diagnostics and other microbiologic testing methods, a causal pathogen can be identified in only half of cases of CAP. This finding highlights that our understanding of CAP pathogenesis is incomplete. As molecular diagnostics become more advanced and use broadens, our knowledge is expected to grow.

● Discovery of the lung microbiome – Historically, the lung has been considered sterile. However, culture-independent techniques (ie, high throughput 16S ribosomal ribonucleic acid [rRNA] gene sequencing) have identified complex and diverse communities of microbes that reside within the alveoli [ 19-21 ]. This finding suggests that resident alveolar microbes play a role in the development of pneumonia, either by modulating the host immune response to infecting pathogens or through direct overgrowth of specific pathogens within the alveolar microbiome. (See 'Pathogenesis' below.)

Antimicrobial resistance  —  Knowledge of antimicrobial resistance patterns and risk factors for infection with antimicrobial-resistant pathogens help inform the selection of antibiotics for empiric CAP treatment ( table 4 ).

● S. pneumoniae may be resistant to one or more antibiotics commonly used for the empiric treatment of CAP.

• Macrolide resistance rates vary regionally but are generally high (>25 percent) in the United States, Asia, and southern Europe. Resistance rates tend to be lower in northern Europe. (See "Resistance of Streptococcus pneumoniae to the macrolides, azalides, and lincosamides" .)

• Estimates of doxycycline resistance are less certain and vary substantially worldwide. In the United States, rates tend to be less than 20 percent but may be rising. (See "Resistance of Streptococcus pneumoniae to the fluoroquinolones, doxycycline, and trimethoprim-sulfamethoxazole" .)

• Beta-lactam resistance rates also vary regionally but to a lesser extent than macrolide and doxycycline resistance. In the United States, <20 percent of isolates are resistant to penicillin and <1 percent to cephalosporins. (See "Resistance of Streptococcus pneumoniae to beta-lactam antibiotics" .)

• Fluoroquinolone resistance tends to be <2 percent in the United States but varies regionally and with specific risk factors such as recent antibiotic use or hospitalization. (See "Resistance of Streptococcus pneumoniae to the fluoroquinolones, doxycycline, and trimethoprim-sulfamethoxazole" .)

Because resistance rates vary even at local levels, clinicians should refer to local antibiograms to guide antibiotic selection when available. General epidemiologic data can be obtained through sources such as the OneHealthTrust (formerly the Center for Disease Dynamics, Economics & Policy [CDDEP]).

● Methicillin-resistant S. aureus (MRSA) is an uncommon cause of CAP. Risk factors for MRSA have two patterns: health care associated and community acquired. The strongest risk factors for MRSA pneumonia include known MRSA colonization or prior MRSA infection, particularly involving the respiratory tract. Gram-positive cocci on sputum Gram stain are also predictive of MRSA infection. Other factors that should raise suspicion for MRSA infection include recent antibiotic use (particularly receipt of intravenous antibiotics within the past three months), recent influenza-like illness, the presence of empyema, necrotizing/cavitary pneumonia, and immunosuppression ( table 4 ).

In contrast with health care-associated MRSA, community-acquired MRSA (CA-MRSA) infections tend to occur in younger healthy persons [ 22 ]. Risk factors for CA-MRSA infection include a history of MRSA skin lesions, participation in contact sports, injection drug use, crowded living conditions, and men who have sex with men. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Epidemiology" .)

CAP caused by CA-MRSA can be severe and is associated with necrotizing and/or cavitary pneumonia, empyema, gross hemoptysis, septic shock, and respiratory failure. These features may be attributable to infection with toxin-producing CA-MRSA strains. In the United States, these strains tend to be methicillin resistant and belong to the USA300 clone. (See "Methicillin-resistant Staphylococcus aureus (MRSA): Microbiology and laboratory detection" .)

● Pseudomonas is also an uncommon cause of CAP and tends to occur more frequently in patients with known colonization or prior infection with Pseudomonas spp, recent hospitalization or antibiotic use, underlying structural lung disease (eg, cystic fibrosis or advanced chronic obstructive pulmonary disease [bronchiectasis]), and immunosuppression. Antibiotic resistance is common among pseudomonal strains, and empiric therapy with more than one agent that targets Pseudomonas is warranted for at-risk patients with moderate to severe CAP ( table 4 ). (See "Pseudomonas aeruginosa pneumonia" and 'Inpatient antibiotic therapy' below.)

PATHOGENESIS  — 

Traditionally, CAP has been viewed as an infection of the lung parenchyma, primarily caused by bacterial or viral respiratory pathogens. In this model, respiratory pathogens are transmitted from person to person via droplets or, less commonly, via aerosol inhalation (eg, as with Legionella or Coxiella species). Following inhalation, the pathogen colonizes the nasopharynx and then reaches the lung alveoli via microaspiration. When the inoculum size is sufficient and/or host immune defenses are impaired, infection results. Replication of the pathogen, the production of virulence factors, and the host immune response lead to inflammation and damage of the lung parenchyma, resulting in pneumonia ( figure 3 ).

With the identification of the lung microbiome, that model has changed [ 19-21 ]. While the pathogenesis of pneumonia may still involve the introduction of respiratory pathogens into the alveoli, the infecting pathogen likely has to compete with resident microbes to replicate. In addition, resident microbes may also influence or modulate the host immune response to the infecting pathogen. If this is correct, an altered alveolar microbiome (alveolar dysbiosis) may be a predisposing factor for the development of pneumonia.

In some cases, CAP might also arise from uncontrolled replication of microbes that normally reside in the alveoli. The alveolar microbiome is similar to oral flora and is primarily comprised of anaerobic bacteria (eg, Prevotella and Veillonella ) and microaerophilic streptococci [ 19-21 ]. Hypothetically, exogenous insults such as a viral infection or smoke exposure might alter the composition of the alveolar microbiome and trigger overgrowth of certain microbes. Because organisms that compose the alveolar microbiome typically cannot be cultivated using standard cultures, this hypothesis might explain the low rate of pathogen detection among patients with CAP.

In any scenario, the host immune response to microbial replication within the alveoli plays an important role in determining disease severity. For some patients, a local inflammatory response within the lung predominates and may be sufficient for controlling infection. In others, a systemic response is necessary to control infection and to prevent spread or complications, such as bacteremia. In a minority, the systemic response can become dysregulated, leading to tissue injury, sepsis, acute respiratory distress syndrome, and/or multiorgan dysfunction.

The pathogenesis of CAP is discussed in greater detail separately. (See "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults" .)

CLINICAL PRESENTATION  — 

The clinical presentation of CAP varies widely, ranging from mild pneumonia characterized by fever, cough, and shortness of breath to severe pneumonia characterized by sepsis and respiratory distress. Symptom severity is directly related to the intensity of the local and systemic immune response in each patient.

● Pulmonary signs and symptoms – Cough (with or without sputum production), dyspnea, and pleuritic chest pain are among the most common symptoms associated with CAP. Signs of pneumonia on physical examination include tachypnea, increased work of breathing, and adventitious breath sounds, including rales/crackles and rhonchi. Tactile fremitus, egophony, and dullness to percussion also suggest pneumonia. These signs and symptoms result from the accumulation of white blood cells (WBCs), fluid, and proteins in the alveolar space. Hypoxemia can result from the subsequent impairment of alveolar gas exchange. On chest radiograph, accumulation of WBCs and fluid within the alveoli appears as pulmonary opacities ( image 1A-B ).

● Systemic signs and symptoms – The great majority of patients with CAP present with fever. Other systemic symptoms such as chills, fatigue, malaise, chest pain (which may be pleuritic), and anorexia are also common. Tachycardia, leukocytosis with a leftward shift, or leukopenia are also findings that are mediated by the systemic inflammatory response. Inflammatory markers, such as the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and procalcitonin may rise, though the latter is largely specific to bacterial infections. CAP is also the leading cause of sepsis; thus, the initial presentation may be characterized by hypotension, altered mental status, and other signs of organ dysfunction such as renal dysfunction, liver dysfunction, and/or thrombocytopenia [ 23 ].

Although certain signs and symptom such as fever, cough, tachycardia, and rales are common among patients with CAP, these features are ultimately nonspecific and are shared among many respiratory disorders (see 'Differential diagnosis' below). No individual symptom or constellation of symptoms is adequate for diagnosis without chest imaging. For example, the positive predictive value of the combination of fever, tachycardia, rales, and hypoxia (oxygen saturation <95 percent) among patients with respiratory complaints presenting to primary care was <60 percent when chest radiograph was used as a reference standard [ 24 ].

Signs and symptoms of pneumonia can also be subtle in patients with advanced age and/or impaired immune systems, and a higher degree of suspicion may be needed to make the diagnosis. As examples, older patients may present with mental status changes but lack fever or leukocytosis [ 25 ]. In immunocompromised patients, pulmonary infiltrates may not be detectable on chest radiographs but can be visualized with computed tomography.

The clinical and diagnostic features of CAP and sepsis are discussed in detail separately. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults" and "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis", section on 'Clinical presentation' .)

Making the diagnosis  —  The diagnosis of CAP generally requires the demonstration of an infiltrate on chest imaging in a patient with a clinically compatible syndrome (eg, fever, dyspnea, cough, and sputum production) [ 26 ].

● For most patients with suspected CAP, we obtain posteroanterior and lateral chest radiographs. Radiographic findings consistent with the diagnosis of CAP include lobar consolidations ( image 1C ), interstitial infiltrates ( image 1D-E ), and/or cavitations ( image 2 ). Although certain radiographic features suggest certain causes of pneumonia (eg, lobar consolidations suggest infection with typical bacterial pathogens), radiographic appearance alone cannot reliably differentiate among etiologies.

● For selected patients in whom CAP is suspected based on clinical features despite a negative chest radiograph, we obtain computed tomography (CT) of the chest. These patients include immunocompromised patients, who may not mount strong inflammatory responses and thus have negative chest radiographs, as well as patients with known exposures to epidemic pathogens that cause pneumonia (eg, Legionella ). Because there is no direct evidence to suggest that CT scanning improves outcomes for most patients and cost is high, we do not routinely obtain CT scans when evaluating patients for CAP.

The combination of a compatible clinical syndrome and imaging findings consistent with pneumonia are sufficient to establish an initial clinical diagnosis of CAP. However, this combination of findings is nonspecific and is shared among many cardiopulmonary disorders. Thus, remaining attentive to the possibility of an alternate diagnosis as a patient's course evolves is important to care. (See 'Differential diagnosis' below.)

Defining severity and site of care  —  For patients with a working diagnosis of CAP, the next steps in management are defining the severity of illness and determining the most appropriate site of care. Determining the severity of illness is based on clinical judgement and can be supplemented by use of severity scores ( algorithm 1 ).

The most commonly used severity scores are the Pneumonia Severity Index (PSI) and CURB-65 [ 27,28 ]. We generally prefer the PSI, also known as the PORT score ( calculator 1 ), because it is the most accurate and its safety and effectiveness in guiding clinical decision-making have been validated [ 29-32 ]. However, the CURB-65 score is a reasonable alternative and is preferred by many clinicians because it is easier to use ( calculator 2 ).

The three levels of severity (mild, moderate, and severe) generally correspond to three levels of care:

● Ambulatory care – Most patients who are otherwise healthy with normal vital signs (apart from fever) and no concern for complication are considered to have mild pneumonia and can be managed in the ambulatory setting. These patients typically have PSI scores of I to II and CURB-65 scores of 0 (or a CURB-65 score of 1 if age >65 years).

● Hospital admission – Patients who have peripheral oxygen saturations <92 percent on room air (and a significant change from baseline) should be hospitalized. In addition, patients with PSI scores of ≥III and CURB-65 scores ≥1 (or CURB-65 score ≥2 if age >65 years) should also generally be hospitalized.

Because patients with early signs of sepsis, rapidly progressive illness, or suspected infections with aggressive pathogens are not well represented in severity scoring systems, these patients may also warrant hospitalization in order to closely monitor the response to treatment.

Practical concerns that may warrant hospital admission include an inability to take oral medications, cognitive or functional impairment, or other social issues that could impair medication adherence or ability to return to care for clinical worsening (eg, substance use, homelessness, or residence far from a medical facility).

● Intensive care unit (ICU) admission – Patients who meet either of the following major criteria have severe CAP and should be admitted to the ICU [ 26 ]:

• Respiratory failure requiring mechanical ventilation

• Sepsis requiring vasopressor support

Recognizing these two criteria for ICU admission is relatively straightforward. The challenge is to identify patients with severe CAP who have progressed to sepsis before the development of organ failure. For these patients, early ICU admission and administration of appropriate antibiotics improve outcomes. To help identify patients with severe CAP before development of organ failure, the American Thoracic Society (ATS) and the Infectious Diseases Society of America (IDSA) suggest minor criteria [ 1,26 ].

The presence of three of these criteria warrants ICU admission:

• Altered mental status

• Hypotension requiring fluid support

• Temperature <36°C (96.8°F)

• Respiratory rate ≥30 breaths/minute

• Arterial oxygen tension to fraction of inspired oxygen (PaO 2 /FiO 2 ) ratio ≤250

• Blood urea nitrogen (BUN) ≥20 mg/dL (7 mmol/L)

• Leukocyte count <4000 cells/microL

• Platelet count <100,000/microL

• Multilobar infiltrates

Although several other scores for identifying patients with severe CAP and/or ICU admission have been developed, we generally use the ATS/IDSA major and minor criteria because they are well validated [ 33-35 ].

Detailed discussion on assessing severity and determining the site of care in patients with CAP is provided separately. (See "Community-acquired pneumonia in adults: Assessing severity and determining the appropriate site of care" .) (Related Pathway(s): Community-acquired pneumonia: Determining the appropriate site of care for adults .)

Triage of patients with known or suspected COVID-19 is also discussed elsewhere. (See "COVID-19: Evaluation of adults with acute illness in the outpatient setting", section on 'Disposition' .)

Microbiologic testing  —  The benefit of obtaining a microbiologic diagnosis should be balanced against the time and cost associated with an extensive evaluation in each patient.

Generally, we take a tiered approach to microbiologic evaluation based on CAP severity and the site of care ( table 5 ):

● Outpatients − For most patients with mild CAP being treated in the ambulatory setting, microbiologic testing is not needed (apart from testing for SARS-CoV-2 during the pandemic). Empiric antibiotic therapy is generally successful, and knowledge of the infecting pathogen does not usually improve outcomes.

● Patients with moderate CAP admitted to the general medicine ward − For most patients with moderate CAP admitted to the general medical ward, we obtain the following:

• Blood cultures

• Sputum Gram stain and culture

• Urinary antigen testing for S. pneumoniae

• Testing for Legionella spp (polymerase chain reaction [PCR] when available, urinary antigen test as an alternate)

• SARS-CoV-2 testing

During the pandemic, we test all patients for COVID-19. During respiratory virus season (eg, late fall to early spring in the northern hemisphere), we also test for other respiratory viruses (eg, influenza, adenovirus, parainfluenza, respiratory syncytial virus, and human metapneumovirus). When testing for influenza, PCR is preferred over rapid antigen testing. (See "Seasonal influenza in adults: Clinical manifestations and diagnosis" .)

For these patients, making a microbiologic diagnosis allows for directed therapy, which helps limit antibiotic overuse, prevent antimicrobial resistance, and reduce unnecessary complications, such as Clostridioides difficile infections.

● Patients with severe CAP (including ICU admission) − For most hospitalized patients with severe CAP, including those admitted to the ICU, we send blood cultures, sputum cultures, urinary streptococcal antigen, and Legionella testing. In addition, we obtain bronchoscopic specimens for microbiologic testing when feasible, weighing the benefits of obtaining a microbiologic diagnosis against the risks of the procedure (eg, need for intubation, bleeding, bronchospasm, pneumothorax) on a case-by-case basis. When pursuing bronchoscopy, we usually send specimens for aerobic culture, Legionella culture, fungal stain and culture, and testing for respiratory viruses.

The type of viral diagnostic tests used (eg, PCR, serology, culture) vary among institutions. In some cases, multiplex PCR panels that test for a wide array of viral and bacterial pathogens are used. While we generally favor using these tests for patients with severe pneumonia, we interpret results with caution as most multiplex assays have not been approved for use on lower respiratory tract specimens. In particular, the detection of single viral pathogen does not confirm the diagnosis of viral pneumonia because viruses can serve as cofactors in the pathogenesis of bacterial CAP or can be harbored asymptomatically.

In all cases, we modify this approach based on epidemiologic exposures, patient risk factors, and clinical features regardless of CAP severity or treatment setting ( table 3 ). As examples:

● For patients with known or probable exposures to epidemic pathogens such as Legionella or epidemic coronaviruses, we broaden our evaluation to include tests for these pathogens. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults", section on 'Important pathogens' .)

● For patients with cavitary pneumonia, we may include testing for tuberculosis, fungal pathogens, and Nocardia .

● For immunocompromised patients, we broaden our differential to include opportunistic pathogens such as Pneumocystis jirovecii , fungal pathogens, parasites, and less common viral pathogens such as cytomegalovirus. The approach to diagnostic testing varies based on the type and degree of immunosuppression and other patient-specific factors. (See "Approach to the immunocompromised patient with fever and pulmonary infiltrates" and "Epidemiology of pulmonary infections in immunocompromised patients" .)

When defining the scope of our microbiologic evaluation, we also take the certainty of the diagnosis of CAP into consideration. Because a substantial portion of patients hospitalized with an initial clinical diagnosis of CAP are ultimately found to have alternate diagnoses [ 17 ], pursuing a comprehensive microbiologic evaluation can help reach the final diagnosis (eg, blood cultures obtained as part of the evaluation for CAP may help lead to a final diagnosis of endocarditis).

Detailed discussion on the microbiologic evaluation of CAP is provided separately. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults" and "Sputum cultures for the evaluation of bacterial pneumonia" .)

The diagnosis of COVID-19 during the pandemic is also discussed in detail elsewhere. (See "COVID-19: Diagnosis" .)

DIFFERENTIAL DIAGNOSIS  — 

CAP is a common working diagnosis and is frequently on the differential diagnosis of patients presenting with a pulmonary infiltrate and cough, patients with respiratory tract infections, and patients with sepsis. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults", section on 'Differential diagnosis' .)

Noninfectious illnesses that mimic CAP or co-occur with CAP and present with pulmonary infiltrate and cough include:

• Congestive heart failure with pulmonary edema

• Pulmonary embolism

• Pulmonary hemorrhage

• Atelectasis

• Aspiration or chemical pneumonitis

• Drug reactions

• Lung cancer

• Collagen vascular diseases

• Vasculitis

• Acute exacerbation of bronchiectasis

• Interstitial lung diseases (eg, sarcoidosis, asbestosis, hypersensitivity pneumonitis, cryptogenic organizing pneumonia)

For patients with an initial clinical diagnosis of CAP who have rapidly resolving pulmonary infiltrates, alternate diagnoses should be investigated. Pulmonary infiltrates in CAP are primarily caused by the accumulation of white blood cells (WBCs) in the alveolar space and typically take weeks to resolve. A pulmonary infiltrate that resolves in one or two days may be caused by accumulation of fluid in the alveoli (ie, pulmonary edema) or a collapse of the alveoli (ie, atelectasis) but not due to accumulation of WBCs.

Respiratory illnesses that mimic CAP or co-occur with CAP include:

• Acute exacerbations of chronic obstructive pulmonary disease

• Influenza and other respiratory viral infections

• Acute bronchitis ( figure 4 )

• Asthma exacerbations

Febrile illness and/or sepsis can also be the presenting syndrome in patients with CAP; other common causes of these syndromes include urinary tract infections, intraabdominal infections, and endocarditis.

TREATMENT  — 

For most patients with CAP and excluding COVID-19, the etiology is not known at the time of diagnosis, and antibiotic treatment is empiric, targeting the most likely pathogens. The pathogens most likely to cause CAP vary with severity of illness, local epidemiology, and patient risk factors for infection with drug-resistant organisms.

As an example, for most patients with mild CAP who are otherwise healthy and treated in the ambulatory setting, the range of potential pathogens is limited. By contrast, for patients with CAP severe enough to require hospitalization, potential pathogens are more diverse, and the initial treatment regimens are often broader. (Related Pathway(s): Community-acquired pneumonia: Empiric antibiotic selection for adults in the outpatient setting and Community-acquired pneumonia: Empiric antibiotic selection for adults admitted to a general medical ward and Community-acquired pneumonia: Empiric antibiotic selection for adults admitted to the intensive care unit .)

The management of COVID-19 is discussed in detail elsewhere. (See "COVID-19: Management in hospitalized adults" and "COVID-19: Management of adults with acute illness in the outpatient setting" .)

Outpatient antibiotic therapy  —  For all patients with CAP, empiric regimens are designed to target S. pneumoniae (the most common and virulent bacterial CAP pathogen) and atypical pathogens. Coverage is expanded for outpatients with comorbidities, smoking, and recent antibiotic use to include or better treat beta-lactamase-producing H. influenzae , M. catarrhalis , and methicillin-susceptible S. aureus . For those with structural lung disease, we further expand coverage to include Enterobacteriaceae, such as E. coli and Klebsiella spp ( algorithm 2 ).

Selection of the initial regimen depends on the adverse effect profiles of available agents, potential drug interactions, patient allergies, and other patient-specific factors.

● For most patients aged <65 years who are otherwise healthy and have not recently used antibiotics, we typically use oral amoxicillin (1 g three times daily) plus a macrolide (eg, azithromycin or clarithromycin ) or doxycycline . Generally, we prefer to use a macrolide over doxycycline.

This approach differs from the American Thoracic Society (ATS)/Infectious Diseases Society of America (IDSA), which recommend monotherapy with amoxicillin as first line and monotherapy with either doxycycline or a macrolide (if local resistance rates are <25 percent [eg, not in the United States]) as alternatives for this population [ 26 ]. The rationale for each approach is discussed separately. (See "Treatment of community-acquired pneumonia in adults in the outpatient setting", section on 'Empiric antibiotic treatment' .)

● For patients who have major comorbidities (eg, chronic heart, lung, kidney, or liver disease, diabetes mellitus, alcohol dependence, or immunosuppression), who are smokers, and/or who have used antibiotics within the past three months, we suggest oral amoxicillin-clavulanate (875 mg twice daily or extended release 2 g twice daily) plus either a macrolide (preferred) or doxycycline .

Alternatives to amoxicillin-based regimens include combination therapy with a cephalosporin plus a macrolide or doxycycline or monotherapy with lefamulin .

● For patients who can use cephalosporins, we use a third-generation cephalosporin (eg, cefpodoxime ) plus either a macrolide or doxycycline .

● For patients who cannot use any beta-lactam, we select a respiratory fluoroquinolone (eg, levofloxacin , moxifloxacin , gemifloxacin) or lefamulin . For those with structural lung disease, we prefer a respiratory fluoroquinolone because its spectrum of activity includes Enterobacteriaceae.

In the absence of hepatic impairment or drug interactions, lefamulin is a potential alternative to fluoroquinolones for most others. However, clinical experience with this agent is limited. Use should be avoided in patients with moderate to severe hepatic dysfunction, known long QT syndrome, or in those taking QT-prolonging agents, pregnant and breastfeeding women, and women with reproductive potential not using contraception. There are drug interactions with CYP3A4 and P-gp inducers and substrates; in addition, lefamulin tablets are contraindicated with QT-prolonging CYP3A4 substrates. Refer to the drug interactions program included within UpToDate.  

Omadacycline is another newer agent that is active against most CAP pathogens, including Enterobacteriaceae. It is a potential alternative for patients who cannot tolerate beta-lactams (or other agents) and want to avoid fluoroquinolones. (See "Treatment of community-acquired pneumonia in adults who require hospitalization", section on 'New antimicrobial agents' .)

Modifications to these regimens may be needed for antibiotic allergy, drug interactions, specific exposures, and other patient-specific factors. In particular, during influenza season, patients at high risk for poor outcomes from influenza may warrant antiviral therapy ( table 6 ).

We treat most patients for five days. However, we generally ensure that all patients are improving on therapy and are afebrile for at least 48 hours before stopping antibiotics. In general, extending the treatment course beyond seven days does not add benefit. Studies supporting this approach are discussed separately. (See "Treatment of community-acquired pneumonia in adults in the outpatient setting", section on 'Duration of therapy' .)

Detailed discussion on the treatment of CAP in the outpatient setting, including antibiotic efficacy data, is provided separately. (See "Treatment of community-acquired pneumonia in adults in the outpatient setting" .) (Related Pathway(s): Community-acquired pneumonia: Empiric antibiotic selection for adults in the outpatient setting .)

Inpatient antibiotic therapy

General medical ward  —  For patients with CAP admitted to the medical ward, empiric antibiotic regimens are designed to treat S. aureus , gram-negative enteric bacilli (eg, Klebsiella pneumoniae ) in addition to typical pathogens (eg, S. pneumoniae , H. influenzae , and M. catarrhalis ) and atypical pathogens (eg, Legionella pneumophilia , M. pneumoniae , and C. pneumoniae ).

We generally start antibiotic therapy as soon as we are confident that CAP is the appropriate working diagnosis and, ideally, within four hours of presentation. Delays in appropriate antibiotic treatment that exceed four hours have been associated with increased mortality [ 36 ].

The key factors in selecting an initial regimen for hospitalized patients with CAP are risk of infection with Pseudomonas and/or methicillin-resistant S. aureus (MRSA). The strongest risk factors for MRSA or Pseudomonas infection are known colonization or prior infection with these organisms, particularly from a respiratory tract specimen. Recent hospitalization (ie, within the past three months) with receipt of intravenous (IV) antibiotics is also a risk factor, particularly for pseudomonal infection. Suspicion for these pathogens should otherwise be based on local prevalence (when known), other patient-specific risk factors, and the overall clinical assessment ( algorithm 3 and table 4 ):

● For patients without suspicion for MRSA or Pseudomonas , we generally use one of two regimens: combination therapy with a beta-lactam plus a macrolide or monotherapy with a respiratory fluoroquinolone [ 26 ]. Because these two regimens have similar clinical efficacy, we select among them based on other factors (eg, antibiotic allergy, drug interactions). For patients who are unable to use either a macrolide or a fluoroquinolone, we use a beta-lactam plus doxycycline .

● For patients with known colonization or prior infection with Pseudomonas, recent hospitalization with IV antibiotic use, or other strong suspicion for pseudomonal infection , we typically use combination therapy with both an antipseudomonal beta-lactam (eg, piperacillin-tazobactam , cefepime , ceftazidime , meropenem , or imipenem ) plus an antipseudomonal fluoroquinolone (eg, ciprofloxacin or levofloxacin ). The selection of empiric regimens should also be informed by the susceptibility pattern for prior isolates.

● For patients with known colonization or prior infection with MRSA or other strong suspicion for MRSA infection , we add an agent with anti-MRSA activity, such as vancomycin or linezolid , to either of the above regimens. We generally prefer linezolid over vancomycin when community-acquired MRSA is suspected (eg, a young, otherwise healthy patient who plays contact sports presenting with necrotizing pneumonia) because of linezolid's ability to inhibit bacterial toxin production [ 37 ]. Ceftaroline is a potential alternative for the treatment of MRSA pneumonia but is not US Food and Drug Administration approved. (See "Treatment of community-acquired pneumonia in adults who require hospitalization", section on 'Community-acquired MRSA' .)

Modifications to initial empiric regimens may be needed for antibiotic allergy, potential drug interactions, current epidemics, specific exposures, resistance patterns of known colonizing organisms or organisms isolated during prior infections, and other patient-specific factors. In particular, antiviral treatment (eg, oseltamivir ) should be given as soon as possible for any hospitalized patient with known or suspected influenza. (See "Seasonal influenza in nonpregnant adults: Treatment" .)

Detailed discussion about antibiotic therapy, including use of new agents (eg, lefamulin , omadacycline ) for patients hospitalized to a general medical ward is provided separately. (See "Treatment of community-acquired pneumonia in adults who require hospitalization" .) (Related Pathway(s): Community-acquired pneumonia: Empiric antibiotic selection for adults admitted to a general medical ward .)

ICU admission

Antibiotic selection  —  For patients with CAP admitted to the intensive care unit (ICU), our approach to antibiotic selection is similar to that used for patients admitted to the general medical ward. However, because of the severity of illness in this population, we do not use monotherapy ( algorithm 4 ). In addition, we start antibiotic therapy within one hour of presentation for patients who are critically ill.

The spectrum of activity of the empiric regimen should be broadened in patients with risk factors for Pseudomonas infection or MRSA infection ( table 4 ).

● For most patients without suspicion for MRSA or Pseudomonas , we treat with a beta-lactam (eg, ceftriaxone , cefotaxime , ceftaroline , ampicillin-sulbactam , ertapenem ) plus a macrolide (eg, azithromycin or clarithromycin ) or a beta-lactam plus a respiratory fluoroquinolone (eg, levofloxacin or moxifloxacin ) [ 26 ].

For patients with penicillin hypersensitivity reactions, we select an appropriate agent (eg, later-generation cephalosporin, carbapenem, or a beta-lactam alternative) based on the type and severity of reaction ( algorithm 5 ). For patients who cannot use any beta-lactam (ie, penicillins, cephalosporins, and carbapenems), we typically use combination therapy with a respiratory fluoroquinolone and aztreonam .

● For patients with known colonization or prior infection with MRSA, recent hospitalization with IV antibiotic use, or other strong suspicion for MRSA infection , we add an agent with anti-MRSA activity, such as vancomycin or linezolid , to either of the above regimens [ 26 ].

● For patients with known colonization or prior infection with Pseudomonas , recent hospitalization with IV antibiotic use, or other strong suspicion for pseudomonal infection , we typically use combination therapy with both an antipseudomonal beta-lactam (eg, piperacillin-tazobactam , cefepime , ceftazidime , meropenem , or imipenem ) plus an antipseudomonal fluoroquinolone (eg, ciprofloxacin or levofloxacin ) for empiric treatment [ 26 ].

For patients with penicillin hypersensitivity reactions, we select an appropriate agent based on the type and severity of penicillin reaction ( algorithm 5 ) and prior pseudomonal susceptibility testing.

Modifications to initial empiric regimens may be needed for antibiotic allergy, potential drug interactions, current epidemics, specific exposures, resistance patterns of colonizing bacteria or bacteria isolated during prior infections, and other patient-specific factors. In particular, antiviral treatment (eg, oseltamivir ) should be given as soon as possible for any hospitalized patient with known or suspected influenza. (See "Seasonal influenza in nonpregnant adults: Treatment" .)

Detailed discussion about antibiotic treatment for patients with CAP admitted to the ICU and patients with sepsis and/or respiratory failure are provided separately. (See "Treatment of community-acquired pneumonia in adults who require hospitalization", section on 'Intensive care unit' and "Evaluation and management of suspected sepsis and septic shock in adults" .) (Related Pathway(s): Community-acquired pneumonia: Empiric antibiotic selection for adults admitted to the intensive care unit .)

Adjunctive glucocorticoids  —  The role of adjunctive glucocorticoid treatment for CAP is evolving. The rationale for use is to reduce the inflammatory response to pneumonia, which may in turn reduce progression to lung injury, ARDS, and mortality. Based on randomized trials, the greatest benefit is for patients with impending respiratory failure or those requiring mechanical ventilation, particularly when glucocorticoids are given early in the course.

● For most immunocompetent patients with respiratory failure due to CAP who require invasive or non-invasive mechanical ventilation or with significant hypoxemia (ie, PaO2:FIO2 ratio <300 with an FiO 2 requirement of ≥50 percent and use of either high flow nasal cannula or a nonrebreathing mask), we suggest continuous infusion of hydrocortisone 200 mg daily for 4 to 7 days followed by a taper. Because mortality benefit appears to be greatest with early initiation, hydrocortisone should ideally be started as soon as possible. The decision to taper glucocorticoids at day 4 or 7 is based on clinical response.

● Because glucocorticoid use may impair the immune control of influenza, tuberculosis, and fungal pathogens, we avoid hydrocortisone use in patients with CAP caused by these pathogens or for patients with concurrent acute viral hepatitis or active herpes viral infection, which may also be worsened with glucocorticoid use.

● For immunocompromised patients, we weigh the risks and benefits of use on an individual basis.

● While we do not treat CAP with adjunctive glucocorticoids in most other circumstances, we do not withhold glucocorticoids when they are indicated for other reasons, including:

• Refractory septic shock (see "Corticosteroid therapy for refractory septic shock in adults" )

• Acute exacerbations of COPD (see "COPD exacerbations: Management", section on 'Glucocorticoids in moderate to severe exacerbations' )

• COVID-19 (see "COVID-19: Management in hospitalized adults", section on 'Dexamethasone and other glucocorticoids' )

Additional detail on the use of glucocorticoids for CAP and review of the evidence are discussed separately. (See "Treatment of community-acquired pneumonia in adults who require hospitalization", section on 'Adjunctive glucocorticoids' .)

Disposition  —  Once a patient with CAP is hospitalized, further management will be dictated by the patient's response to initial empiric therapy. Clinical response should be assessed during daily rounds. While various criteria have been proposed to assess clinical response [ 38-40 ], we generally look for subjective improvement in cough, sputum production, dyspnea, and chest pain. Objectively, we assess for resolution of fever and normalization of heart rate, respiratory rate, oxygenation, and white blood cell count. Generally, patients demonstrate some clinical improvement within 48 to 72 hours ( table 7 ).

Antibiotic de-escalation  —  For patients in whom a causative pathogen has been identified, we tailor therapy to target the pathogen [ 41 ]. If coverage for MRSA was added empirically, and MRSA was not identified as a pathogen nor on a screening nasal swab and the patient is improving, we typically discontinue the anti-MRSA agent (eg, vancomycin ). However, for the majority of patients hospitalized with CAP, a causative pathogen is not identified. For these patients, we continue empiric treatment for the duration of therapy, provided that the patient is improving. Intravenous antibiotic regimens can be transitioned to oral regimens with a similar spectrum activity as the patient improves ( algorithm 6 ) [ 42,43 ].

Duration of therapy  —  We generally determine the duration of therapy based on the patient's clinical response to therapy.

For all patients, we treat until the patient has been afebrile and clinically stable for at least 48 hours and for a minimum of five days. Patients with mild infection generally require five to seven days of therapy. Patients with severe infection or chronic comorbidities generally require 7 to 10 days of therapy. Extended courses may be needed for immunocompromised patients, patients with infections caused by certain pathogens (eg, P. aeruginosa) , or those with complications. (See "Treatment of community-acquired pneumonia in adults who require hospitalization", section on 'Duration of therapy' .)

In accord with the ATS/IDSA, we do not use procalcitonin to help determine whether to start antibiotics [ 26 ]. However, we sometimes use procalcitonin thresholds as an adjunct to clinical judgment to help guide antibiotic discontinuation in clinically stable patients. We generally obtain a level at the time of diagnosis and repeat the level every one to two days in patients who are clinically stable. We determine the need for continued antibiotic therapy based on clinical improvement and serial procalcitonin levels ( algorithm 7 ). (See "Procalcitonin use in lower respiratory tract infections" .)

Discharge  —  Hospital discharge is appropriate when the patient is clinically stable, 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 to oral therapy. Early discharge based on clinical stability and criteria for switching to oral therapy is encouraged to reduce risk associated with prolonged hospital stays and unnecessary cost.

Immunocompromised patients  —  The spectrum of potential pathogens expands considerably in immunocompromised patients to include invasive fungal infections, less common viral infections (eg, cytomegalovirus), and parasitic infections (eg, toxoplasmosis) [ 44 ].

The risk for specific infections varies with the type and degree of immunosuppression and whether the patient is taking prophylactic antimicrobials. As examples, prolonged neutropenia, T cell immunosuppression, and use of tumor necrosis factor-alpha inhibitors predispose to invasive fungal infections (eg, aspergillosis, mucormycosis) as well as mycobacterial infections. Advanced human immunodeficiency virus (HIV) infection (eg, CD4 cell count <200 cells/microL), prolonged glucocorticoid use (particularly when used with certain chemotherapeutics), and lymphopenia each should raise suspicion for pneumocystis pneumonia. Multiple infections may occur concurrently in this population, and the likelihood of disseminated infection is greater. Because signs and symptoms of infection can be subtle and nonspecific in immunocompromised patients, diagnosis can be challenging and invasive procedures are often required for microbiologic diagnosis. Broad-spectrum empiric therapy may be needed prior to obtaining a specific microbiologic diagnosis [ 45 ].

Because management is complex, drug interactions are common, adjustments in immunosuppressive regimens may be needed, and empiric treatment options (eg, amphotericin B) can be associated with significant toxicity, we generally involve a multidisciplinary team of specialists when caring for immunocompromised patients with pneumonia. (See "Epidemiology of pulmonary infections in immunocompromised patients" and "Approach to the immunocompromised patient with fever and pulmonary infiltrates" and "Tumor necrosis factor-alpha inhibitors: Bacterial, viral, and fungal infections" .)

FOLLOW-UP IMAGING  — 

Most patients with clinical resolution after treatment do not require a follow-up chest radiograph, as radiographic response lags behind clinical response. However, follow-up clinic visits are good opportunities to review the patient's risk for lung cancer based on age, smoking history, and recent imaging findings ( algorithm 8 ).

This approach is similar to that outlined by the ATS/IDSA, which recommend not obtaining a follow-up chest radiograph in patients whose symptoms have resolved within five to seven days [ 26 ]. (See "Treatment of community-acquired pneumonia in adults who require hospitalization", section on 'Follow-up chest radiograph' .)

COMPLICATIONS AND PROGNOSIS  — 

While most patients with CAP will recover with appropriate antibiotic treatment, some will progress and/or develop complications despite appropriate therapy (ie, clinical failure) and some will remain symptomatic (ie, nonresolving pneumonia).

Clinical failure  —  Clear indicators of clinical failure include progression to sepsis and/or respiratory failure despite appropriate antibiotic treatment and respiratory support. Other indicators include an increase in subjective symptoms (eg, cough, dyspnea) usually in combination with objective criteria (eg, decline in oxygenation, persistent fever, or rising white blood cell). Various criteria have been proposed to define clinical failure but none widely adopted [ 46-48 ].

Reasons for clinical failure generally fall into these categories:

● Progression of the initial infection – For some patients, CAP can lead to overwhelming infection despite appropriate antibiotic treatment. In some, this indicates a dysregulated host immune response. In others, this may indicate that the infection has spread beyond the pulmonary parenchyma (eg, empyema, lung abscess, bacteremia, endocarditis).

Other possibilities include infection with a drug-resistant pathogen or an unusual pathogen not covered by the initial empiric antibiotic regimen. Alternatively, failure to respond to treatment may signify the presence of an immunodeficiency (eg, new diagnosis of HIV infection).

● Development of comorbid complications – Comorbid complications may be infectious or noninfectious. Nosocomial infections, particularly hospital-acquired pneumonia (HAP), are common causes of clinical failure. In addition to HAP, others include catheter-related bloodstream infections, urinary tract infections, and C. difficile infection [ 49 ].

Cardiovascular events are also common complications and include acute myocardial infarction, cardiac arrhythmias, congestive heart failure, pulmonary embolism, and stroke [ 50-52 ]. Older age, preexisting cardiovascular disease, severe pneumonia, and infection with certain pathogens (ie, S. pneumoniae and influenza) have each been associated with increased risk of cardiovascular events [ 50,53-55 ]. Recognition that cardiovascular events and other systemic complications can occur during the acute phase of CAP is also changing our view of CAP from an acute pulmonary process to an acute systemic disease. (See "Morbidity and mortality associated with community-acquired pneumonia in adults", section on 'Cardiac complications' .)

Because of these possibilities, we generally broaden our initial antibiotic regimen for patients who are progressing despite appropriate empiric treatment and evaluate for alternate diagnoses, less common or drug-resistant pathogens, and/or infectious and cardiovascular complications. (See 'Differential diagnosis' above and "Morbidity and mortality associated with community-acquired pneumonia in adults" .)

Nonresolving CAP  —  For some patients, initial symptoms will neither progress nor improve with at least seven days of appropriate empiric antibiotic treatment. We generally characterize these patients as having nonresolving pneumonia. Potential causes of nonresolving CAP include:

● Delayed clinical response – For some patients, particularly those with multiple comorbidities, severe pneumonia, bacteremia, and infection with certain pathogens (eg, S. pneumoniae ), treatment response may be slow. Eight or nine days of treatment may be needed before clinical improvement is evident.

● Loculated infection – Patients with complications such as lung abscess, empyema, or other closed space infections may fail to improve clinically despite appropriate antibiotic selection. Such infections may require drainage and/or prolonged antibiotic treatment. (See "Lung abscess in adults" and "Epidemiology, clinical presentation, and diagnostic evaluation of parapneumonic effusion and empyema in adults" .)

● Bronchial obstruction – Bronchial obstruction (eg, by a tumor) can cause a postobstructive pneumonia that may fail to respond or slowly respond to standard empiric antibiotic regimens for CAP.

● Pathogens that cause subacute/chronic CAP – Mycobacterium tuberculosis , nontuberculous mycobacteria (eg, Mycobacterium kansasii ), fungi (eg, Histoplasma capsulatum , Blastomyces dermatitidis ), or less common bacteria (eg, Nocardia spp, Actinomyces israelii ) can cause subacute or chronic pneumonia that may fail to respond or may incompletely respond to standard empiric antibiotic regimens for CAP.

● Incorrect initial diagnosis – Failure to improve despite seven days of treatment also raises the possibility of an alternate diagnosis (eg, malignancy or inflammatory lung disease). (See 'Differential diagnosis' above.)

Once a patient is characterized as having nonresolving CAP, a complete new physical examination, laboratory evaluation, imaging studies, and microbiologic workup will be necessary to define the etiology of nonresolving CAP [ 49 ]. Initiation of workup for nonresolving CAP should not be automatically associated with a change in initial empiric antibiotic therapy. (See "Nonresolving pneumonia" .)

Long-term complications and mortality  —  Although the majority of patient with CAP recover without complications, CAP is a severe illness and among the leading causes of mortality worldwide. Mortality can be directly attributable to CAP (eg, overwhelming sepsis or respiratory failure) or can result indirectly from cardiovascular events or other comorbid complications (eg, advanced chronic obstructive pulmonary disease [COPD]) [ 56 ].

Long-term complications resulting from pneumonia are increasingly recognized and there is a shift in the medical community to define pneumonia as a systemic illness that can lead to chronic disease [ 57 ]. While the precise incidence of long-term complications is not known, the more common long-term sequelae involve the respiratory tract and cardiovascular system [ 58 ].

In the United States, pneumonia (combined with influenza) is among the top 10 most common causes of death [ 5 ]. Thirty-day mortality rates vary with disease severity, ranging from less than 1 percent in ambulatory patients to approximately 20 to 25 percent in patients with severe CAP. In addition to disease severity, older age, comorbidities (eg, COPD, diabetes mellitus, cardiovascular disease), infection with certain pathogens (eg, S. pneumoniae ), and acute cardiac complications are each associated with increased short-term mortality [ 50,59,60 ].

CAP is also associated with increased long-term mortality [ 7,61-63 ]. In one population-based study evaluating 7449 patients hospitalized with CAP, mortality rates were 6.5 percent during hospitalization, 13 percent 30 days after hospitalization, 23 percent at six months after hospitalization, and 31 percent at one year after hospitalization [ 7 ]. During the same study year, an estimated 1,581,860 patients were hospitalized in the United States. Extrapolating mortality data to these patients, the number of deaths in the United States population will be 102,821 during hospitalization, 205,642 at 30 days, 370,156 at six months, and 484,050 at one year [ 7 ]. Causes of long-term mortality are primarily related to comorbidities and include malignancy, COPD, and cardiovascular disease [ 56 ].

Data associating CAP with long-term mortality indicate that CAP is not only a common cause of acute morbidity and mortality but also a disease with important chronic health outcomes.

PREVENTION  — 

The primary pillars for the prevention of CAP are [ 64-66 ]:

● Smoking cessation (when appropriate)

● Influenza vaccination for all patients

● Pneumococcal vaccination for at-risk patients

● Vaccination against SARS-CoV-2

Each is discussed in detail separately. (See "Overview of smoking cessation management in adults" and "Seasonal influenza vaccination in adults" and "Pneumococcal vaccination in adults" and "COVID-19: Vaccines" .)

The United States Centers for Disease Control and Prevention provides online  clinician  and  patient  resources for all seasonal respiratory viral vaccinations.

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 5 th to 6 th 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 10 th to 12 th 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 email 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 topic (see "Patient education: Pneumonia in adults (The Basics)" )

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

SUMMARY AND RECOMMENDATIONS

● Background – Community-acquired pneumonia (CAP) is a leading cause of morbidity and mortality worldwide. (See 'Incidence' above.)

● Risk factors – Risk factors include age ≥65 years, chronic comorbidities, concurrent or antecedent respiratory viral infections, impaired airway protection, smoking, excess alcohol use, and other lifestyle factors (eg, crowded living conditions). (See 'Risk factors' above.)

● Microbiology – The most commonly identified causes of CAP include respiratory viruses (particularly severe acute respiratory syndrome coronavirus 2 during the pandemic), typical bacteria (eg, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis ) and atypical bacteria (eg, Legionella spp, Mycoplasma pneumoniae, Chlamydia pneumoniae ). Pseudomonas and methicillin-resistant Staphylococcus aureus (MRSA) are less common causes that predominantly occur in patients with specific risk factors. (See 'Microbiology' above and 'Pathogenesis' above.)

● Making the diagnosis – Diagnosis requires demonstration of an infiltrate on chest imaging in a patient with a clinically compatible syndrome (eg, fever, dyspnea, cough, and leukocytosis). For most patients, a posteroanterior and lateral chest radiograph is sufficient. Computed tomography scan is reserved for selected cases. (See 'Clinical presentation' above and 'Making the diagnosis' above.)

● Alternate and concurrent diagnoses – While the combination of a compatible clinical syndrome and an infiltrate on chest imaging are sufficient to establish an initial clinical diagnosis of CAP, these findings are nonspecific. Remaining attentive to the possibility of an alternate or concurrent diagnosis as a patient's course evolves is important to care. (See 'Differential diagnosis' above.)

● Determining severity of illness – For patients with a working diagnosis of CAP, the initial steps in management are defining the severity of illness and determining the most appropriate site of care ( algorithm 1 ). For most patients, we determine our approach to microbiologic testing based on this assessment ( table 5 ). (See 'Microbiologic testing' above.)

● Empiric antibiotic selection – The selection of an empiric antibiotic regimen is based on the severity of illness, site of care, and most likely pathogens. We generally start antibiotics as soon as we are confident that CAP is the appropriate working diagnosis and, ideally, within four hours of presentation for inpatients and within one hour of presentation for those who are critically ill (see 'Treatment' above):

• For most outpatients, we prefer to use combination therapy with a beta-lactam and either a macrolide (preferred) or doxycycline . Alternatives to beta-lactam-based regimens include monotherapy with either a fluoroquinolone or, alternatively, lefamulin or omadacycline (newer agents). Selection among these agents depends on patient comorbidities, drug interactions, allergies, and other intolerances. Clinical experience with lefamulin and omadacycline are limited; warnings and contraindications exist ( algorithm 2 ).

This approach differs from the American Thoracic Society/Infectious Diseases Society of America, which recommend monotherapy with amoxicillin as first line and monotherapy with either doxycycline or a macrolide (if local resistance rates are <25 percent [eg, not in the United States]) as alternatives for this population.

• For most inpatients admitted to the general medical ward, treatment options include either intravenous (IV) combination therapy with a beta-lactam plus a macrolide or doxycycline or monotherapy with a respiratory fluoroquinolone ( algorithm 3 ). These regimens should be expanded for patients with risk factors for Pseudomonas or MRSA ( table 4 ).

• For most patients admitted to the intensive care unit (ICU), treatment options include IV combination therapy with a beta-lactam plus either a macrolide or a respiratory fluoroquinolone ( algorithm 4 ). As with other hospitalized patients, regimens should be expanded for patients with risk factors for Pseudomonas or MRSA ( table 4 ).

● Adjunctive glucocorticoids – The benefit of adjunctive glucocorticoids appears greatest in patients with impending respiratory failure or requiring mechanical ventilation, particularly when they are given early in the course. Generally, we add hydrocortisone for most immunocompetent patients with respiratory failure due to CAP who require invasive or non-invasive mechanical ventilation or with significant hypoxemia (ie, PaO2:FIO2 ratio <300 with an FiO 2 requirement of ≥50 percent and use of either high flow nasal cannula or a nonrebreathing mask), unless there are reason to avoid their use (eg, infection with certain pathogen [influenza, fungi, tuberculosis, or immunocompromise]). (See 'Adjunctive glucocorticoids' above.)

● Directed antibiotic therapy – For patients in whom a causative pathogen has been identified, we tailor therapy to target the pathogen. (See 'Antibiotic de-escalation' above.)

● Duration of antibiotics – For all patients, we treat until the patient has been afebrile and clinically stable for at least 48 hours and for a minimum of five days. Patients with mild infection generally require five to seven days of therapy; those with severe infection or chronic comorbidities generally require 7 to 10 days of therapy. (See 'Duration of therapy' above.)

● Lack of response to antibiotics – Failure to respond to antibiotic treatment within 72 hours should prompt reconsideration of the diagnosis and empiric treatment regimen as well as an assessment for complications. (See 'Clinical failure' above and 'Nonresolving CAP' above.)

● Prevention – Key preventive measures include smoking cessation (when appropriate), influenza vaccination for the general population, and pneumococcal vaccination for at-risk populations. (See 'Prevention' above.)

ACKNOWLEDGMENT  — 

UpToDate gratefully acknowledges John G Bartlett, MD, who contributed as Section Editor on earlier versions of this topic and was a founding Editor-in-Chief for UpToDate in Infectious Diseases.

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