eMedicine Specialties > Infectious Diseases > Lower Respiratory Tract Infections

Pneumonia, Community-Acquired

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Updated: Jul 24, 2009

Introduction

Background

Community-acquired pneumonia (CAP) is one of the most common infectious diseases addressed by clinicians. CAP is an important cause of mortality and morbidity worldwide.

Pathophysiology

CAP is usually acquired via inhalation or aspiration of pulmonary pathogenic organisms into a lung segment or lobe. Less commonly, CAP results from secondary bacteremia from a distant source, such as Escherichia coli urinary tract infection and/or bacteremia. CAP due to aspiration of oropharyngeal contents is the only form of CAP involving multiple pathogens.

Frequency

United States

Patients who require hospital treatment for CAP are typically elderly persons and those with underlying chronic obstructive pulmonary disease (COPD), such as chronic bronchitis (not emphysema). CAP is a common cause of hospital admission, but statistics of patients treated for CAP in the ambulatory setting are difficult to obtain. Overall, the incidence of CAP in 1994 was 170 cases per 10,000 individuals.

International

The prevalence of zoonotic CAPs is higher internationally than in the United States.

Mortality/Morbidity

• Patients with severe CAP invariably have severe cardiopulmonary disease or diminished or absent splenic function.
• Mortality and morbidity rates of CAP are highest in elderly patients.

Race

CAP has no racial predilection.

Sex

CAP has no sexual predilection.

Age

CAP is particularly common in elderly adults, with an incidence rate in the United States of 280 cases per 10,000 individuals older than 65 years.

Clinical

History

Patients with community-acquired pneumonia (CAP) due to typical bacterial pathogens present with various pulmonary symptoms, while those with CAP due to atypical pathogens present with a variety of both pulmonary and extrapulmonary symptoms.

• Patients with bacterial CAP typically present with variable degrees of fever, usually with a productive cough and often with pleuritic chest pain.
• The clinical presentation of CAP due to atypical pathogens is usually less acute than CAP due to typical bacterial pathogens.
• CAP due to atypical pathogens may have one or more extrapulmonary features, which is a clue to their presence.
• Patients with Legionella pneumonia may have a productive or nonproductive cough. In contrast, patients with pneumonia due to Mycoplasma pneumoniae or Chlamydia pneumoniae usually present with a nonproductive cough.
• With the exception of Legionella pneumonia, chest pain is typically not a feature of CAP due to nonzoonotic atypical pathogens.

Physical

• Abnormal physical findings are confined to the chest in patients with typical bacterial CAP.
• Rales are heard upon auscultation of the chest over the involved lobe or segment. If consolidation is present, an increase in tactile fremitus, bronchial breathing, and E to A change may be present.
• Pleural effusion (usually due to Haemophilus influenzae infection) that is large enough produces signs that are detectable during physical examination. Patients with pleural effusion have decreased tactile fremitus and dullness upon chest percussion. Pleural effusion in a patient with CAP and extrapulmonary manifestations should suggest Legionella infection. Pleural effusion with appropriate epidemiologic history findings, such as contact with a rabbit or deer, may suggest tularemia.
• Purulent sputum is characteristic of pneumonia caused by typical bacterial pathogens but is typically not a feature of that caused by atypical pathogens, with the exception of Legionnaires disease.
• Blood-tinged sputum may be found in patients with pneumococcal infections, Klebsiella pneumonia, or Legionella pneumonia.
• Legionella pneumonia, Q fever, and psittacosis are atypical pneumonias that may present with signs of consolidation. Consolidation is not a feature of pneumonia caused by M pneumoniae or C pneumoniae.
• Patients with CAP who present with acute heart failure, such as acute myocardial infarction without pre-existing congestive heart failure (CHF), often have normal cardiac silhouettes, bilateral symmetric moist rales, and an S3 gallop rhythm upon auscultation.
• Severe CAP is caused by the same spectrum of pathogens that cause mild or moderately severe CAP.
  • The severity of CAP is determined by the pre-existing function of the heart, lungs, and spleen.
  • The severity of CAP depends on host factors rather than on the type, number, or virulence of the involved pathogens. However, with all other factors being equal, influenza, severe acute respiratory syndrome (SARS), hantavirus pulmonary syndrome (HPS), and Legionnaires disease are not likely to present as severe CAP.

Causes

• Typical bacterial pathogens
  • Typical bacterial pathogens that cause CAP include Streptococcus pneumoniae (both penicillin-sensitive and -resistant strains; see Image 1), H influenzae (both ampicillin-sensitive and -resistant strains; see Image 2), and Moraxella catarrhalis (all strains penicillin-resistant; see Image 3). These 3 pathogens account for approximately 85% of CAP cases.
    
    

    

    Gram stain showing Streptococcus pneumoniae.

    
    
    

    

    Gram stain showing Haemophilus influenzae.

    
    
    

    

    Gram stain showing Moraxella catarrhalis.

    
    
    • In patients with chronic bronchitis who develop CAP requiring hospitalization, M catarrhalis infection is particularly common.
    • S pneumoniae remains the most common agent responsible for CAP.
  • Importantly, Staphylococcus aureus, Klebsiella pneumoniae, and Pseudomonas aeruginosa are not causes of CAP in typical hosts.
    • S aureus causes CAP in the setting of postviral influenza.
    • K pneumoniae CAP occurs primarily in persons with chronic alcoholism.
    • P aeruginosa is a cause of CAP in patients with bronchiectasis or cystic fibrosis.
  • Other gram-negative pathogens rarely cause CAP.
  • Aspiration pneumonia is caused by the aspiration of oropharyngeal secretions into the lung. The extent of aspiration and lobar distribution of the infiltrates depends on the patient's position at the time of aspiration.
  • Nearly all cases of CAP are due to a single pathogen. Exceptions occur but are rare.
  • Aspiration pneumonia is the only form of CAP caused by multiple pathogens.
• Atypical pathogens
  • Atypical pneumonias can be divided into zoonotic and nonzoonotic atypical pathogens.
  • Zoonotic atypical pathogens that cause CAP include Chlamydia psittaci (psittacosis), Francisella tularensis (tularemia), and Coxiella burnetii (Q fever).
    • Contact with the appropriate vector is required for these zoonotic pathogens to cause CAP.
    • A history of close contact with a parturient cat or sheep should be sought in patients with suspected Q fever.
    • Psittacosis is preceded by recent close contact with psittacine birds.
    • Patients with tularemia have had recent close contact with deer or rabbits or have recently been bitten by a tick or deer fly.
  • Nonzoonotic atypical pneumonias are caused by Legionella species, M pneumoniae, or C pneumoniae. These 3 pathogens account for approximately 15% of all CAP cases. Legionella species are the most important atypical pathogens that cause CAP.
  • Typical and atypical pneumonias are differentiated based on the pattern of extrapulmonary findings rather than on individual findings.
  • Typical bacterial pneumonias produce few, if any, extrapulmonary findings. In contrast, each atypical pathogen has its own distribution pattern of extrapulmonary organ involvement, which permits an accurate and rapid presumptive clinical diagnosis (see Image 4).
    
    

    

    Clinical diagnostic approach in community-acquired pneumonias.

    
    
  • Table 1. Differential Diagnostic Features of Atypical Pneumonias¹

    	Zoonotic Atypical Pneumonias			Nonzoonotic Atypical Pneumonias
    Key Characteristics	Psittacosis	Q Fever	Tularemia	Mycoplasma Pneumonia	Legionnaires Disease	Chlamydia Pneumonia
    Symptoms
    Mental confusion	—	—	—	±	+	—
    Prominent headache	+	+	—	—	—	—
    Meningismus	+	—	—	—	—	±
    Myalgias	+	+	—	+	+	—
    Ear pain	—	—	—	±	—	—
    Pleuritic pain	—	—	—	±	+	—
    Abdominal pain	—	—	—	—	+	—
    Diarrhea	—	—	—	±	+	—
    Signs
    Rash	± (Horder spots)	—	—	± (erythema multiforme)	±	—
    Raynaud phenomenon	—	—	—	±	—	—
    Nonexudative pharyngitis	+	—	±	+	—	+
    Hemoptysis	+	—	—	—	+	—
    Lobar consolidation	±	±	±	±	±	—
    Cardiac involvement	± (endocarditis)	± (myocarditis)		± (myocarditis/ heart block/ pericarditis)	— (endocarditis, myocarditis)
    Splenomegaly	+	+	—	—	—	—
    Relative bradycardia	+	±	—	—	+	—
    Chest Film
    Infiltrate	Patchy/ consolidation	Patchy/ consolidation	Ovid bodies	Patchy	Patchy/ consolidation	Single circumscribed lesions
    Bilateral hilar adenopathy	—	—	+	—	—	—
    Pleural effusion	—	—	+ (bloody)	± (small)	± (small/ moderate)	±

  • Although Q fever and psittacosis are associated with relative bradycardia, these zoonotic pneumonias may be excluded by a negative epidemiologic vector contact history finding.
  • If psittacosis and Q fever are eliminated from the diagnostic consideration by history, relative bradycardia in a patient with CAP should suggest Legionnaires disease.
    • Because Legionella pneumonia has its own characteristic pattern of organ involvement, it is readily distinguished from other typical and atypical pathogens (see Image 7).
      
      

      

      This graph outlines a case of Legionella pneumonia, showing characteristics of bradycardia and extrapulmonary involvement. Also shown is an initial lack of response to beta-lactam antibiotics, followed by effective treatment with doxycycline.

      
      
    • Some signs and symptoms are more important than others and can be expressed in a weighted diagnostic point system, which is highly accurate in assisting the clinician with determining a clinical diagnosis of Legionnaires disease (see Table 3).
  • Table 2. Relative Bradycardia
    
    

    Determination and Evaluation of Relative Bradycardia
    Inclusive criteria	The patient must be an adult (>12 y).
    	The patient must have a fever >101°F.
    	The pulse must be taken while the patient’s temperature is elevated.
    Exclusive criteria	The patient has normal sinus rhythm without arrhythmia, second- or third-degree heart block, or pacemaker-induced rhythm.
    	Patient must not be receiving a beta-blocker, verapamil, or diltiazem.
    Temperature-Pulse Relationships (temperature and corresponding pulse [beats/min])
    Appropriate Pulse	Relative Bradycardia
    41.1°C/106°F = 150/min	<140/min
    40.6°C/105°F = 140/min	<130/min
    40.0°C/104°F = 130/min	<120/min
    39.5°C/103°F = 120/min	<110/min
    38.9°C/102°F = 110/min	<100/min
    Causes of Relative Bradycardia
    Infectious causes	Legionella infection Psittacosis Q fever Typhoid fever Typhus Malaria Babesiosis Leptospirosis Yellow fever Dengue fever Rocky Mountain spotted fever Tularemia Salmonella infections
    Noninfectious causes	Beta-blockers CNS lesions Lymphomas Factitious fever Drug fever

  • Another clue to Legionnaires disease in a patient with CAP and relative bradycardia is the lack of response to beta-lactam antibiotic treatment. If other causes of relative bradycardia are excluded, this is a clue because it is a constant early finding in Legionnaires disease.
  • Table 3. Modified Winthrop University Hospital Infectious Disease Division's Point System for Diagnosing Legionnaires Disease in Adults¹
    
    

    Clinical Features	Qualifying Conditions	Point Score
    Temperature >103°F*	With relative bradycardia	+5
    Headache	Acute onset	+2
    Mental confusion/lethargy*	Not drug-induced	+4
    Ear pain	Acute onset	-3
    Nonexudative pharyngitis	Acute onset	-3
    Hoarseness	Acute, not chronic	-3
    Sputum (purulent)	Excluding chronic bronchitis	-3
    Hemoptysis*	Mild/moderate	-3
    Chest pain (pleuritic)	Rapidly progressive asymmetrical infiltrates* (excluding severe influenza/SARS)	-3
    Loose stools/watery diarrhea*	Not drug induced	+3
    Abdominal pain*	With or without diarrhea	+5
    Renal failure*	Acute, not chronic	+5
    Shock/hypotension*	Not 2° to acute cardiac	-5
    	/pulmonary causes	+5
    Splenomegaly	Excluding non-CAP causes	-5
    Lack of response to beta lactams	After 72 h (excluding viral pneumonias)	+5
    Laboratory Features
    Chest radiography	Rapidly progressive asymmetrical infiltrates* (excluding severe influenza/SARS)	+3
    ↓ PO2 with ↑ A-a gradient (>35)*	(Excluding severe influenza/SARS)	-5
    ↓ Na +	Acute onset	+1
    ↓ PO4 =*	Acute onset	+5
    ↑ SGOT/SGPT (early mild/transient)*	Acute onset	+4
    ↑ Total bilirubin	Otherwise unexplained	+1
    ↑ LDH (>400)*	Excluding HIV/PCP	-5
    ↑ CPK/aldolase	Otherwise unexplained	+4
    ↑ CRP (>30)	Acute onset	+5
    ↑ Cold agglutinins (≥1:64)	Acute onset	-5
    ↑ Creatinine	Acute onset	+2
    Microscopic hematuria*	Excluding trauma, BPH, Foley catheter, bladder/renal neoplasms	+2
    Likelihood of Legionella Infection
    Total Points	>15, Legionella infection very likely
    	5-15, Legionella infection likely
    	<5 Legionella infection unlikely

    
    *Otherwise unexplained (acute and associated with pneumonia)
  • In typical hosts, CAP does not present with shock. If CAP presents with shock, look for impaired or absent splenic function. Disorders and therapies associated with impaired splenic function include the following:²
    • Chronic alcoholism
    • Amyloidosis
    • Chronic active hepatitis
    • Fanconi syndrome
    • Hyposplenism in elderly patients
    • Immunoglobulin A (IgA) deficiency
    • Intestinal lymphangiectasia
    • Myeloproliferative disorders
    • Waldenström macroglobulinemia
    • Non-Hodgkin lymphoma
    • Celiac disease
    • Regional enteritis
    • Sézary syndrome
    • Congenital asplenia
    • Splenectomy
    • Sickle cell trait/disease
    • Splenic infarcts
    • Splenic malignancies
    • Steroid therapy
    • Rheumatoid arthritis
    • Systemic lupus erythematosus (SLE)
    • Systemic mastocytosis
    • Systemic necrotizing vasculitis
    • Thyroiditis
    • Pulmonary embolism
    • Congestive heart failure or acute myocardial infarction
  • CAP that presents with shock in the absence of conditions associated with hyposplenism should prompt an evaluation for mimics of pneumonia that manifest as pulmonary infiltrates on chest radiography, fever, leukocytosis, and hypotension, such as acute myocardial infarction or acute pulmonary embolism.
  • If CAP manifests as shock without evidence of hyposplenia, acute myocardial infarction, or acute pulmonary embolism, consider an exacerbation of pre-existing cardiopulmonary disease that presents with hypotension and coronary insufficiency with hypoxemia or emphysema.
• Nonpulmonary pathogens that have been known to cause CAP include the following:
  • Nonaeruginosa pseudomonads
  • Stenotrophomonas (Xanthomonas) maltophilia
  • Citrobacter freundii
  • Burkholderia (Pseudomonas) cepacia
  • Citrobacter koseri
  • Enterobacter species
  • Flavobacterium species
  • Enterobacter cloacae
  • Flavobacterium meningisepticum
  • Enterobacter agglomerans
  • Enterococcus species

Differential Diagnoses

Chronic Bronchitis
Myocardial Infarction

Other Problems to Be Considered

Congestive Heart Failure and Pulmonary Edema
Asthma
Myocardial infarction precipitated by fever due to community-acquired pneumonia (CAP)
Tracheobronchitis
SLE pneumonitis
Acute drug hypersensitivity reactions (nitrofurantoin)
Pulmonary embolus or infarction
Bronchogenic carcinoma

Workup

Laboratory Studies

• Send the sputum of patients with community-acquired pneumonia (CAP) for Gram stain and/or culture. Keep in mind that many patients, especially elderly persons, are not able to produce an adequate suitable sputum sample.
  • Gram stain shows few or no predominant organisms in patients with Legionnaires disease and purulent sputum.
  • Do not send the sputum of patients with COPD (eg, chronic bronchitis) for Gram stain or culture because these patients invariably demonstrate a mixed or normal flora.
• Obtain 2 or 3 sets of blood cultures from all patients with CAP upon admission because some typical bacterial pathogens, such as S pneumoniae and H influenzae, are frequently associated with positive blood culture findings. M catarrhalis bacteremia is unusual.
• Presentation with CAP and extrapulmonary findings suggests atypical pathogens. Workup should include serum transaminase levels, serum phosphorous levels, urinalysis, and cold agglutinin titers.
  • Otherwise unexplained early, transient, and slight increases in serum transaminases in a patient with CAP suggest the presence of psittacosis, Q fever, or Legionella pneumonia.
  • Otherwise unexplained hypophosphatemia in a patient with CAP suggests Legionnaires disease.
  • Otherwise unexplained microscopic hematuria in a patient with CAP also suggests Legionnaires disease.
• Low-titer cold agglutinin elevations occur in various viral and neoplastic illnesses. Of patients with Mycoplasma pneumonia, 75% develop transient elevations of cold agglutinins early in the course of the illness.
  • A negative cold agglutinin titer finding does not exclude Mycoplasma species.
  • A moderately elevated cold agglutinin titer effectively rules out Legionella pneumonia. Because low titer elevations of cold agglutinins are nonspecific, the diagnosis of Mycoplasma pneumonia is likely only if the cold agglutinin titer is highly elevated (>1:64) in a patient with CAP.
  • In a patient with CAP, the higher the cold agglutinin titer (>1:64), the more likely the cold agglutinins are due to Mycoplasma species.
• In a patient with suspected Legionella pneumonia, direct fluorescent antibody (DFA) testing of the sputum can assist in diagnosis if obtained early and before antimicrobial treatment. Antimicrobial treatment rapidly decreases the sputum yield of DFA testing (see Image 5).
  
  

  

  Sputum direct fluorescent antibody stain showing Legionella infection.

  
  
• Send serology if zoonotic atypical pathogens are suspected because isolation and culture are difficult and dangerous for microbiology personnel. Diagnosis of zoonotic pathogen–associated pneumonia is based on a 4-fold or greater increase in titers between acute- and convalescent-phase serum specimens.
• Obtain immunoglobulin M (IgM) and immunoglobulin G (IgG) titers for C pneumoniae and M pneumoniae if they are a diagnostic possibility. An increase in the IgG titer for either organism suggests past exposure and does not indicate acute infection. An increase in the IgM titer for either pathogen allows the diagnosis in a patient with CAP.
• Obtain Legionella serologies if Legionella pneumonia is suggested based on the pattern of extrapulmonary findings. However, negative acute titer findings do not rule out Legionnaires disease because titers may not rise for 6-8 weeks. The finding of an initially high Legionella titer is unusual, and clinical diagnosis rests on demonstrating a 4-fold or greater increase between acute- and convalescent-phase titers.
• The Legionella urine antigen test is applicable only for the Legionella pneumophila serogroup type I, which accounts for approximately 80% of infections. The urinary antigen test remains positive for Legionella for long periods but may be negative early in the infection.
• If C pneumoniae infection is suspected, obtain specific pneumonia IgM and IgG titers. Do not obtain chlamydial titers without specifying the species.
• Approach CAP in patients with HIV infection as follows:
  • The pathogen responsible for CAP in patients with HIV infection is determined by the CD4 count. The differential diagnoses of the pathogen are determined by assessing the CD4 count and the chest radiographic appearance in patients with HIV infection (see Image 8).
    
    

    

    Chest radiograph in a patient with HIV infection, bilateral perihilar infiltrates, and Pneumocystis carinii pericarditis.

    
    
  • Patients with HIV infection and a normal or slightly decreased CD4 count with focal infiltrates have approximately the same pathogen distribution as typical hosts. Patients with nonfocal infiltrates or hypoxemia may have Pneumocystis (carinii) jiroveci pneumonia when the CD4 count is decreased appropriately. Patients with HIV infection, very low CD4 counts, and focal infiltrates commonly have tuberculosis, which is easily diagnosed using an acid-fast bacillus smear of sputum (see Image 6, Image 9).
    
    

    

    A case of Legionnaires disease from the Philadelphia outbreak, showing characteristics of relative bradycardia and extrapulmonary involvement.

    
    
    

    

    Chest radiograph in a patient with HIV infection and focal infiltrates due to tuberculosis.

    
    
  • In patients with HIV infection in whom S pneumoniae CAP is suspected, shell antigen capture assay may be useful.

Imaging Studies

• Obtain chest radiography in all patients with suspected CAP.
  • Obtain chest radiography to exclude conditions that mimic CAP and to confirm the presence of an infiltrate compatible with the presentation of CAP.
  • Patients presenting very early with CAP may have negative findings on chest radiography. In these patients, repeat chest radiography within 24 hours.
  • Chest radiography assists with the differentiation of viral pneumonias from nonviral pneumonias. Viral pneumonias display few or no infiltrates on chest radiography, but, when present, infiltrates are almost always bilateral, perihilar, symmetric, and interstitial. Bacterial pneumonias have a predominantly focal segmental or lobar distribution.
  • In contrast, typical or atypical pathogens produce a lobar or segmental pattern on chest radiography, with or without consolidation or pleural effusion.
  • Chest radiographic findings should be negative in patients with asthma who do not have CAP. Chest radiography findings are also negative in patients with chronic bronchitis.
  • The infiltrates observed with CHF appear as increased interstitial markings and vascular redistribution to the upper lobes. Patients with pre-existing heart failure usually have cardiomegaly.
  • Rapid cavitation is not a typical feature of CAP.
  • Community-acquired methicillin-resistant S aureus (CA-MRSA) CAP presents as a fulminant CAP with rapid cavitation and necrotizing pneumonia caused by CA-MRSA (SCC mec IV) with the PVL gene, which follows influenza.
  • Aspiration pneumonitis may develop cavitation 1 week after aspiration. Signs of cavitation are absent on the initial chest radiograph in patients with CAP due to aspiration.
• Serial chest radiography can be used to observe the progression of CAP.
  • Rapidly progressive asymmetric infiltrates suggest the possibility of Legionnaires disease.
  • Chest radiographic findings worsen rapidly and require a significant period to improve. Clinical resolution occurs long before radiologic resolution.
• Obtain a CT scan of the chest when an underlying bronchogenic carcinoma is suggested or if any abnormalities are not consistent with the diagnosis of pneumonia only.

Procedures

• Diagnostic bronchoscopy with bronchoalveolar lavage (BAL) may be used in patients with CAP when Pneumocystis pneumonia (PCP) is a likely diagnostic possibility.
• Diagnostic bronchi with BAL may also be useful in unresolving CAP that does not respond to appropriate therapy after 3 days.
• Transtracheal aspiration (TTA) is a potentially hazardous procedure and offers no additional diagnostic information in patients with CAP.
• Transthoracic fine-needle aspiration of the infiltrate can be performed and is less hazardous than TTA; however, transthoracic fine-needle aspiration offers no additional information beyond that obtainable via other available diagnostic measures. This procedure is most useful in assessing the cause of noninfectious-associated infiltrates that are not responding to antibiotic treatment.

Histologic Findings

Lung sections with typical bacterial pneumonias show the progression from red hepatization to white hepatization during the resolution process. The lung is repaired after bacterial pneumonia is complete and the infectious process resolves.

Treatment

Medical Care

Therapeutic principles in community-acquired pneumonia

• Pathogens
  • Single pathogens almost always cause community-acquired pneumonia (CAP). Multiple pathogens rarely, if ever, cause CAP.
  • CAP is almost never caused by more than one typical or two atypical organisms or multiple typical/atypical organisms. Studies that report multiple pathogens are flawed and demonstrate one organism microbiologically with serologic evidence of prior exposure to the other pathogen. Clinical experience has demonstrated this principle for decades.
  • The only cause of multiple-pathogen pneumonia is aspiration pneumonia.
• Comorbid conditions
  • Comorbid conditions do not affect selection of antimicrobial therapy.
  • Monotherapy is as effective as multidrug therapy.
  • The addition and/or change of antibiotics based on severity of illness and/or comorbidities is irrational.
  • Antimicrobial therapy is directed against the pathogen rather than against the comorbid factors.
  • Comorbidity is an important prognostic factor and contributes to the severity index but has no place in antibiotic selection.
• Severity
  • The severity of CAP is determined by underlying conditions of the lungs, heart, and spleen.
  • Do not change antibiotics or use additional antibiotics to treat severe CAP.
  • Additional antibiotics do not affect the pulmonary, cardiac, or splenic dysfunction that determines clinical severity.
  • CAP that presents with hypotension and/or shock is due to underlying lung disease, cardiac disease, acute myocardial infarction, or an exacerbation of CHF.
  • Antibiotic monotherapy is the same for mild, moderate, or severe CAP.
  • Rapid cavitation is not a typical feature of CAP. CA-MRSA CAP presents as a fulminant CAP with rapid cavitation and necrotizing pneumonia caused by CA-MRSA (SCC mec IV) with the PVL gene, which follows influenza.
• Appropriate empiric coverage
  • In normal hosts, therapy does not need to cover S aureus, Klebsiella species, or P aeruginosa in CAP. (Most CAP regimens include K pneumoniae coverage.) S aureus coverage should be included in patients with influenza who have focal infiltrates.
  • Most antibiotics used to treat community-acquired aspiration pneumonia (eg, doxycycline, respiratory quinolones, beta-lactams) are highly effective against oral anaerobes. Metronidazole and clindamycin are usually unnecessary. For aerobic lung abscesses, clindamycin or moxifloxacin is preferable.
  • Coverage should include the typical (S pneumoniae, H influenzae, M catarrhalis) and atypical (Legionella and Mycoplasma species, C pneumoniae) pathogens.
• Therapeutic considerations
  • Monotherapy coverage of both typical and atypical pathogens in CAP is preferred over double-drug therapy.
  • Monotherapy is less expensive and as effective as double-drug regimens.
  • Avoid empiric macrolide monotherapy because approximately 25% of S pneumoniae strains are naturally resistant to all macrolides.
  • Preferred monotherapy for CAP includes doxycycline or a respiratory quinolone.
    • This is the least expensive way to optimally treat CAP.
    • No increased resistance is noted with extensive use.
    • No serious adverse effects are noted.
    • It is well tolerated in both oral and intravenous forms.
    • It is ideal for intravenous-to-oral switch monotherapy in terms of patient compliance, safety, and cost.
  • In patients with CAP who are able to take oral medication, switch from intravenous to oral administration after 48 hours, using an antibiotic with the appropriate spectrum, high bioavailability, minimal adverse gastrointestinal effect profile, little or no resistance potential, and relatively low cost such as doxycycline or a respiratory quinolone.
  • Most penicillin resistance is relative resistance and is readily treatable with penicillin and/or beta-lactams.
  • Most highly penicillin-resistant S pneumoniae infections (minimum inhibitory concentration [MIC] >2 µg/mL) may also be treated with beta-lactams. Alternately, doxycycline or respiratory quinolones may be used. Vancomycin is rarely, if ever, needed.
  • Very highly penicillin-resistant S pneumoniae (MIC 6 µg/mL) strains are a rare cause of CAP but remain susceptible to ceftriaxone.

Treatment measures

• Patients with CAP who are moderately to severely ill should be hospitalized. Factors that predict an increased risk of mortality in patients with CAP have been studied and include older age, significant comorbidities, increased respiratory rate, hypotension, fever, multilobar involvement, anemia, and hypoxia, among others.
• Patients with severe CAP require admission to an intensive care unit (ICU). Oxygen and/or ventilatory support may be required.
• Because the severity of CAP frequently is due to underlying severe cardiopulmonary disease, direct medical efforts at supporting cardiopulmonary function while administering antibiotics for CAP.
• Patients admitted with severe CAP and hypotension or shock are often hypotensive because of an acute pulmonary or cardiac insult such as pulmonary embolism or acute myocardial infarction.
• If no acute cardiopulmonary explanation can be found (eg, exacerbation of severe underlying lung disease, exacerbation of pre-existing CHF), patients with shock likely have diminished or absent splenic function.
  • Many underlying conditions are associated with diminished splenic function that may manifest as severe CAP (see Causes).
  • An abdominal scar due to abdominal trauma or lymphoma staging is a probable sign that the patient has asplenia.
  • Howell-Jolly bodies in the peripheral blood smear in a patient presenting with CAP who is in shock suggest hyposplenism. The first step in treating a patient in shock is effective intravascular volume replacement. If aggressive intravascular replacement is inadequate, pressors may be added. Do not administer pressors before adequate volume replacement because effective intracirculating intravascular volume will decrease and the blood pressure will drop further.
• Treatment of penicillin-resistant pneumococcal pneumonia is as follows:
  • The overuse of beta-lactam and macrolide antibiotics has probably caused a gradual increase in the S pneumoniae MIC. This relative increase in the MIC (ie, intermediate resistance or relative resistance) can be overcome by using full recommended doses of beta-lactams.
  • Most cases of penicillin-resistant S pneumoniae infection are still treated with penicillin. Most strains have increased MICs but are still susceptible and are not clinically resistant to penicillin.
  • Penicillin resistance is classified according to MICs. Breakpoints are as follows:
    • Sensitive - 0.6 µg/mL or less
    • Intermediate resistance - 0.1-1 µg/mL
    • Highly resistant - 2 µg/mL or more
  • Strains of pneumococci that are highly resistant to penicillin may be treated with levofloxacin, the only quinolone indicated for the treatment of highly penicillin-resistant S pneumoniae. Alternatively, vancomycin, clindamycin, or linezolid may be used.
  • The use of non-C cell-wall active agents against S pneumoniae, such as doxycycline or levofloxacin, does not increase penicillin resistance among pneumococci.
  • The widespread use of macrolides and trimethoprim-sulfamethoxazole (TMP-SMX) and tetracycline (excluding doxycycline) has been associated with penicillin-resistant S pneumoniae and multidrug-resistant S pneumoniae. 
  • Most oral cephalosporins, except cefprozil, have been associated with increased S pneumoniae resistance. Use of intravenous-to-oral switch programs is as follows:
    • Most patients with CAP who are admitted to the hospital are treated with empiric intravenous antibiotic therapy. Unless these patients are acutely ill in the ICU or are unable to absorb medication from the gastrointestinal tract, they may be switched to equivalent oral therapy to complete a 2-week course of therapy after 48 hours.
    • Candidate agents for intravenous-to-oral switch programs have the same spectrum as intravenous agents, excellent bioavailability, few adverse effects, low resistance potential, and relatively low cost. Ideal agents for intravenous-to-oral switch programs include a respiratory quinolone or doxycycline.
  • Other agents that may be used if S pneumoniae is not the etiologic agent include azithromycin or clarithromycin.

• Monotherapy
  • Ceftriaxone
    • Covers typical pathogens but not atypical pathogens
    • Adverse effects - Non– Clostridium difficile diarrhea, pseudobiliary lithiasis
    • 1 g IV q24h
  • Azithromycin
    • Fails to cover approximately 25% of S pneumoniae strains
    • Should not be used alone
    • Covers atypical pathogens
    • Adverse effects - Nausea, vomiting, non– C difficile diarrhea
    • Very low serum levels - Slow onset/delayed therapeutic effect
    • Moderately expensive
• Combination therapy
  • Ceftriaxone plus erythromycin
    • Covers typical and atypical organisms
    • Adverse effects - Nausea, vomiting, non– C difficile diarrhea, phlebitis, cardiac effects (QTc), pseudobiliary lithiasis
    • Most expensive combination
    • Intravenous-to-oral switch therapy - Disadvantage of double-drug therapy (relatively expensive/inconvenient)
  • Ceftriaxone plus azithromycin
    • Covers typical and atypical pathogens
    • Adverse effects - Nausea, vomiting, non– C difficile diarrhea, phlebitis, cardiac effects (QTc), pseudobiliary lithiasis
    • Intravenous-to-oral switch therapy - Disadvantage of double-drug therapy (relatively expensive/inconvenient)

• Monotherapy
  • Typical CAP pathogens
    • Respiratory quinolone
    • Ceftriaxone
    • Ertapenem
  • Typical CAP pathogens
    • Respiratory quinolone
    • Doxycycline

• CAP in a patient with focal infiltrate on chest radiography and a CD4 count that exceeds 200 cells/µL
  • The most likely pathogens include S pneumoniae, H influenzae, M legionella, or C pneumoniae.
  • Optimal empiric therapy in the context of extrapulmonary findings (atypical pathogens) is with respiratory quinolone or doxycycline. In the absence of extrapulmonary findings (typical bacteria), ceftriaxone, doxycycline, respiratory quinolone, or ertapenem should be used. In patients with CAP who have features of both typical and atypical pathogens, respiratory quinolone or doxycycline should be used.
• CAP in a patient with focal infiltrate on chest radiography and a very low CD4 count (<200 cells/µL)
  • The most likely pathogens include P jiroveci, M tuberculosis, Mycobacterium avium-intracellulare, and Histoplasma capsulatum.
  • Optimal empiric therapy for tuberculosis consists of isoniazid, ethambutol, rifampin, or pyrazinamide. M avium-intracellulare infections are treated with azithromycin plus ethambutol and/or rifampin, rifabutin, or azithromycin plus ethambutol plus respiratory quinolone. Histoplasmosis is treated with itraconazole or amphotericin B.

Consultations

Patients with severe CAP should have the benefit of an infectious disease specialist to assist in the underlying cause of severe CAP.

Diet

Diet in patients with CAP is as tolerated.

Activity

Patients with mild CAP may be treated in an ambulatory setting. Guide activity with common sense.

Medication

Before the role of atypical pathogens was appreciated, most patients with community-acquired pneumonia (CAP) were treated with a parenteral beta-lactam antibiotic. Approximately 15% of patients with possible atypical pneumonias were treated empirically with erythromycin or doxycycline.

Approximately 85% of CAP cases are caused by typical pathogens, such as S pneumoniae, H influenzae, or M catarrhalis, and approximately 15% are due to the nonzoonotic atypical pathogens, such as Legionella species, Mycoplasma species, or C pneumoniae. Atypical pathogens, such as Legionella species, were found to be important causes of CAP. Because clinicians could not clinically differentiate typical pneumonias from atypical pneumonias, combination therapy with a beta-lactam, such as ceftriaxone, in addition to erythromycin to cover both typical and atypical pathogens, became popular.

Although clinically differentiating the typical from the atypical pneumonias with a reasonable degree of certainty is possible, many clinicians empirically treat patients with CAP for both atypical and typical pathogens. Presently, a preferred therapeutic approach to CAP is monotherapy with a respiratory quinolone such as levofloxacin.

The severity of CAP determines the route of antibiotic administration (ie, oral for mild cases, intravenous for moderate-to-severe cases), predicts the necessity of admission to an ICU, predicts the duration of hospital stay, and contributes to the prognosis.

Because patients with CAP have the same pathogen distribution regardless of clinical severity, the empiric antibiotic treatment for CAP does not vary.

Because the severity of CAP is determined by cardiopulmonary or splenic function, using different antibiotics for severe or less severe cases of CAP or adding additional antibiotics because the patient has severe CAP is illogical. Antimicrobial therapy is directed against the microorganism and does not improve cardiopulmonary or splenic function, regardless of the degree of severity.

Antibiotic, Penicillin & Beta-lactamase Inhibitor

Amoxicillin and clavulanate (Augmentin, Augmentin XR)

Amoxicillin inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins. Addition of clavulanate inhibits beta-lactamase–producing bacteria.
Good alternative antibiotic for patients allergic or intolerant to the macrolide class. Usually well tolerated and provides good coverage to most infectious agents. Not effective against Mycoplasma and Legionella species. The half-life of oral dosage form is 1-1.3 h. Has good tissue penetration but does not enter cerebrospinal fluid.
For children > 3 months, base dosing protocol on amoxicillin content. Because of different amoxicillin/clavulanic acid ratios in 250-mg tab (250/125) vs 250-mg chewable tab (250/62.5), do not use 250-mg tab until child weighs >40 kg.
Indicated for CAP caused by beta-lactamase–producing bacteria with reduced susceptibility to penicillin (eg, H influenzae, M catarrhalis, S pneumoniae). The extended-release product is available as amoxicillin 1000 mg and clavulanate 62.5 mg.

Dosing

Adult

Extended-release: Amoxicillin 2 g/clavulanate 125 mg (ie, 2 extended-release tabs) PO q12h for 7-10 d

Pediatric

<3 months: 125 mg/5mL PO susp based on amoxicillin; 30 mg/kg/d divided bid for 7-10 d
>3 months: If using 200 mg/5 mL or 400 mg/5 mL susp, 45 mg/kg/d PO q12h; if using 125 mg/5 mL or 250 mg/5 mL suspension, 40 mg/kg/d PO q8h for 7-10 d
>40 kg: Administer as in adults

Interactions

Coadministration with warfarin or heparin increases risk of bleeding; may act synergistically against selected microorganisms when coadministered with aminoglycosides; coadministration with allopurinol may increase incidence of amoxicillin rash; may decrease efficacy of oral contraceptives when administered concomitantly

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatic impairment may occur with prolonged treatment in elderly patients; diarrhea may occur; adjust dose in renal impairment; cross-allergy may occur with other beta-lactams and cephalosporins

Antibiotic, Tetracycline Derivative

Doxycycline (Vibramycin)

Much more active than tetracycline against many pathogens. Different adverse effect profile and pharmacokinetics than tetracycline. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing arrest of RNA-dependent protein synthesis.

Dosing

Adult

100-200 mg PO/IV q12h

Pediatric

<8 years: Not recommended
>8 years: 2-5 mg/kg/d PO/IV in 1-2 divided doses; not to exceed 200 mg/d

Interactions

Bioavailability minimally decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate

Contraindications

Documented hypersensitivity; avoid in pregnancy and children <8 y

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Rarely, if ever, causes photosensitivity; use during tooth development (last one half of pregnancy through 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines

Antibiotic, Quinolone

Levofloxacin (Levaquin)

For pseudomonal infections and infections due to multidrug resistant gram-negative organisms.

Dosing

Adult

500 mg PO qd for 7-14 d

Pediatric

<18 years: Not recommended
>18 years: Administer as in adults

Interactions

Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; levofloxacin reduces therapeutic effects of phenytoin; probenecid may increase levofloxacin serum concentrations

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy

Moxifloxacin (Avelox)

Inhibits the A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription. Indicated for CAP, including multidrug-resistant S pneumoniae.

Dosing

Adult

400 mg PO/IV qd

Pediatric

<18 years: Not recommended
>18 years: Administer as in adults

Interactions

Antacids, electrolyte supplements reduce absorption; loop diuretics, probenecid, cimetidine increase serum levels; NSAIDs enhance CNS-stimulating effect
May increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT); ferrous sulfate decreases bioavailability (administer moxifloxacin 4 h prior or 8 h following ferrous sulfate); coadministration with drugs that prolong QTc interval (quinidine, procainamide, amiodarone, sotalol, erythromycin, tricyclic antidepressants) increase risk of life-threatening arrhythmia

Contraindications

Documented hypersensitivity; known QT prolongation, concurrent administration of drugs that cause QT prolongation

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); superinfections may occur with prolonged or repeated antibiotic therapy; fluoroquinolones have induced seizures in CNS disorders and caused tendinitis or tendon rupture

Antibiotic, Carbapenem

Ertapenem (Invanz)

Bactericidal activity results from inhibition of cell wall synthesis and is mediated through ertapenem binding to penicillin-binding proteins. Stable against hydrolysis by various beta-lactamases including penicillinases, cephalosporinases, and extended-spectrum beta-lactamases. Hydrolyzed by metallo-beta-lactamases.

Dosing

Adult

1 g qd for 14 d if IV and 7 d if IM; infuse over 30 min if IV
CrCl <30 mL/min/1.73 m²: 500 mg IV qd

Pediatric

<3 months: Not established
3 months to 12 years: 15 mg/kg IV q12h; not to exceed 1 g/d
>12 years: Administer as in adults

Interactions

Probenecid may reduce renal clearance of ertapenem and increase half-life but benefit is minimum and does not justify coadministration

Contraindications

Documented hypersensitivity to drug or amide-type anesthetics

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Pseudomembranous colitis may occur; seizures and CNS adverse reactions may occur; when using with lidocaine to administer intramuscularly, avoid inadvertent injection into blood vessel; decrease dose in renal failure; serious and occasionally fatal hypersensitivity reactions may occur with beta lactams, caution with previous hypersensitivity reactions to penicillin, cephalosporins, other beta lactams, or other allergens; do not mix or co-infuse in same IV line as other medications; do not mix with dextrose-containing diluents

Antibiotic, Macrolide

Azithromycin (Zithromax)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing arrest of RNA-dependent protein synthesis.

Dosing

Adult

500 mg IV q24h for 3 d, then 500 mg/d PO for 7-10 d

Pediatric

<6 months: Not established
>6 months:
Day 1: 10 mg/kg PO once; not to exceed 500 mg/d
Days 2-5: 5 mg/kg PO qd; not to exceed 250 mg/d

Interactions

May cause QT prolongation with cisapride, itraconazole, sparfloxacin, and other medications (probably very rare); may increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine

Contraindications

Documented hypersensitivity; hepatic impairment; do not administer with pimozide

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Site reactions can occur with IV route; may increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function or prolonged QT intervals; caution in patients who are hospitalized, elderly, or debilitated; misses 25% of S pneumoniae

Antibiotic, Cephalosporin (third Generation)

Ceftriaxone (Rocephin)

Third-generation cephalosporin that has broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. Arrests bacterial cell-wall synthesis and inhibits bacterial growth by binding to one or more of the penicillin-binding proteins.

Dosing

Adult

2 g IV q12-24h; not to exceed 4 g/d

Pediatric

Neonates > 7 d: 25-50 mg/kg/d IV/IM; not to exceed 125 mg/d
Infants and children: 100 mg/kg/d IV/IM divided q12h; not to exceed 2 g/d

Interactions

Probenecid may decrease clearance, causing an increase in ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Pseudobiliary lithiasis (sludge in gallbladder) can lead to cholecystectomy; use has been associated with diarrhea that is not caused by C difficile; caution in breastfeeding and in those with penicillin allergy

Follow-up

Further Inpatient Care

Patients with community-acquired pneumonia (CAP) who have severe cardiopulmonary disease or hyposplenic dysfunction have a prolonged course that may require transfer to a subacute unit with less-intensive care.

Further Outpatient Care

Monitor patients with mild CAP treated on an outpatient basis to be sure that they are compliant with their medications and that they are improving. After 1 week, a repeat visit and chest radiography is advisable. As long as the patient is improving and parapneumonic complications are not evident, posttherapy chest radiography is unnecessary.

Inpatient & Outpatient Medications

• Most patients with CAP who are admitted to the hospital are treated with intravenous medications for 2 days and then complete a 12-day oral course of therapy for a total of 14 days of combined intravenous and oral therapy.
• Patients who are severely ill or are unable to tolerate or absorb oral medications require a longer duration of intravenous therapy before switching to an oral antibiotic.
• Mild to moderately ill patients with CAP may be treated entirely via the oral route, either on an inpatient or outpatient basis. Patients receiving oral antibiotics may be admitted for hospital services (eg, pulmonary toilet and additional diagnostic tests) that are not obtainable on an outpatient basis.
• If the patient is switched to an oral regimen and is doing well, earlier discharge from the hospital is possible. The oral therapy regimen can be completed at home.
• Most typical hosts with CAP may be treated with a total 14-day course of medication. Very healthy young adults and children may be treated for shorter periods. Debilitated patients with CAP (eg, those with underlying disorders, compromised hosts) may require longer periods of treatment based on clinical response.
• Optimal intravenous-to-oral switch therapy consists of a single agent that has an appropriate spectrum, has excellent bioavailability, is well tolerated, has a low resistance potential, and is relatively inexpensive.

Deterrence/Prevention

• Pneumococcal vaccines prevent pneumococcal bacteremia but not necessarily pneumococcal pneumonia.
• Nonleukopenic compromised hosts, such as those with rheumatoid arthritis, SLE, or alcoholism, may not develop an antibody response to the pneumococcal vaccine and may therefore remain susceptible to pneumococcal pneumonia. The same is true concerning the use of the Haemophilus vaccine.

Complications

• S pneumoniae pneumonia may be complicated by pleural effusion and/or empyema. Cavitation is not a feature of pneumococcal pneumonia. Bacteremia is part of the disease process and is not a complication of pneumococcal pneumonia.
• K pneumoniae infections, which occur only in patients with chronic alcoholism, may also be complicated by empyema. Cavitation due to Klebsiella infection is a normal part of the disease process and should not be viewed as a complication. Bacteremia is part of the disease process and is not a complication of Klebsiella pneumonia.
• Pleural effusion caused by H influenzae infection is part of the disease process and should not be viewed as a complication.
• M catarrhalis is not typically associated with bacteremia, pleural effusions, or empyema; however, M catarrhalis CAP in a patient with advanced lung disease may prove fatal because of the host’s underlying pulmonary condition.
• Extrapulmonary manifestations associated with M pneumoniae infection should be considered part of the disease process rather than as complications. M pneumoniae infection may result in short-term or permanent asthma.
• As with Mycoplasma pneumonia, Chlamydia pneumonia may be followed or complicated by short-term or long-term bronchospasm. A theory has been suggested that upper respiratory tract infections with C pneumoniae infections may be associated with acute coronary events or coronary artery disease.

Prognosis

• The severity and prognosis of CAP depends primarily on host factors, such as the status of the cardiopulmonary system and splenic function. Obviously, when all other factors are equal, older patients do not fare as well as younger adults.
• Patients with CAP who have impaired splenic function may develop overwhelming pneumococcal sepsis, potentially leading to death within 12-24 hours, regardless of the antimicrobial regimen used.
• Negative prognostic factors include pre-existing lung disease, underlying cardiac disease, advanced age, multilobar involvement, and delayed initiation of appropriate antimicrobial therapy.

Patient Education

• Remind patients with CAP to comply with the medication even after they experience clinical improvement. Except in patients with heart failure, adequate hydration and preservation of the cough reflex during the convalescent period are important.
• For excellent patient education resources, visit eMedicine's Pneumonia Center. Also, see eMedicine's patient education article Bacterial Pneumonia.

Miscellaneous

Medicolegal Pitfalls

Be wary when a patient presents with severe community-acquired pneumonia (CAP), with or without hypotension or shock. In these patients, be sure to exclude an underlying acute pulmonary or cardiac event that could explain the severity of the CAP. In addition, if the severity of CAP or hypotension is not apparently due to cardiopulmonary factors, consider unrelated conditions that may present in a similar clinical fashion, such as acute gastrointestinal bleeding, pancreatitis, or adrenal insufficiency.

Special Concerns

• Do not administer or prescribe tetracyclines to pregnant patients or patients younger than 10 years. Although not approved by the US Food and Drug Administration for patients younger than 18 years, short courses of fluoroquinolones are safe in children who are not very young (ie, <6 y).
• When diagnosing CAP, first exclude other pulmonary conditions that may mimic the clinical presentation of CAP.
  • Newly onset CHF or an exacerbation of pre-existing CHF may result in cough or shortness of breath, which is commonly confused with CAP.
  • Fever due to CAP may precipitate a silent or symptomatic myocardial infarction, which, in turn, may be complicated by CHF.
  • Unless CAP precipitates CHF, CHF and CAP do not coexist simultaneously at clinical presentation.
  • Differentiate an exacerbation of chronic bronchitis or tracheobronchitis from CAP. Because both conditions present with pulmonary symptoms, low-grade fever, and purulent sputum, these conditions may initially be confused with CAP; however, in patients with bronchitis, chest radiography should reveal no infiltrates in the presence of bronchitis.
  • Various other noninfectious disorders occasionally mimic CAP, such as SLE pneumonitis, acute drug hypersensitivity reactions (nitrofurantoin), and pulmonary embolus or infarction.
  • Bronchogenic carcinoma may mimic CAP. In addition, bronchiogenic carcinoma may predispose to CAP by causing bronchial obstruction, resulting in postobstructive pneumonias that do not respond to appropriate antibiotics.
  • Asthma may be precipitated by infection or, less commonly, complicated by CAP. Chest radiography readily helps differentiate asthma from CAP because no infiltrates are present on the chest radiograph in patients with asthma.

Multimedia

Media file 1: Gram stain showing Streptococcus pneumoniae.

Media file 2: Gram stain showing Haemophilus influenzae.

Media file 3: Gram stain showing Moraxella catarrhalis.

Media file 4: Clinical diagnostic approach in community-acquired pneumonias.

Media file 5: Sputum direct fluorescent antibody stain showing Legionella infection.

Media file 6: A case of Legionnaires disease from the Philadelphia outbreak, showing characteristics of relative bradycardia and extrapulmonary involvement.

Media file 7: This graph outlines a case of Legionella pneumonia, showing characteristics of bradycardia and extrapulmonary involvement. Also shown is an initial lack of response to beta-lactam antibiotics, followed by effective treatment with doxycycline.

Media file 8: Chest radiograph in a patient with HIV infection, bilateral perihilar infiltrates, and Pneumocystis carinii pericarditis.

Media file 9: Chest radiograph in a patient with HIV infection and focal infiltrates due to tuberculosis.

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Keywords

community-acquired pneumonia, CAP, bacterial pneumonia, viral pneumonia, pneumococcal pneumonia, Streptococcus pneumoniae pneumonia, S pneumoniae pneumonia, Streptococcus pneumonia, streptococcal pneumonia, Haemophilus influenzae pneumonia, pneumonia, Moraxella catarrhalis pneumonia, M catarrhalis pneumonia, pneumonia, zoonotic pneumonia, pneumonia, pneumonia, Mycoplasma pneumonia pneumonia, pneumonia, pneumonia, Legionnaires disease, tularemia, Q fever, psittacosis, aspiration pneumonia

Contributor Information and Disclosures

Author

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Medical Editor

Fred A Lopez, MD, Associate Professor and Vice Chair, Department of Medicine, Assistant Dean for Student Affairs, Louisiana State University School of Medicine
Fred A Lopez, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, Infectious Diseases Society of America, and Louisiana State Medical Society
Disclosure: Nothing to disclose.

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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Charles V Sanders, MD, Edgar Hull Professor and Chairman, Department of Internal Medicine, Professor of Microbiology, Immunology and Parasitology, Louisiana State University School of Medicine at New Orleans; Medical Director, Medicine Hospital Center, Charity Hospital and Medical Center of Louisiana at New Orleans; Consulting Staff, Ochsner Medical Center
Charles V Sanders, MD is a member of the following medical societies: Alliance for the Prudent Use of Antibiotics, Alpha Omega Alpha, American Association for the Advancement of Science, American Association of University Professors, American Clinical and Climatological Association, American College of Physician Executives, American College of Physicians, American Federation for Medical Research, American Foundation for AIDS Research, American Geriatrics Society, American Lung Association, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Association for Professionals in Infection Control and Epidemiology, Association of American Medical Colleges, Association of American Physicians, Association of Professors of Medicine, Infectious Disease Society for Obstetrics and Gynecology, Infectious Diseases Society of America, Louisiana State Medical Society, Orleans Parish Medical Society, Royal Society of Medicine, Sigma Xi, Society of General Internal Medicine, Southeastern Clinical Club, Southern Medical Association, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology
Disclosure: Nothing to disclose.

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD, Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center
Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Association of Professors of Medicine, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation
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