AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

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

Frequency

United States

Elderly individuals and patients with chronic obstructive pulmonary disease (COPD), such as chronic bronchitis (not emphysema), most frequently are admitted to the hospital for CAP. CAP is a common cause of hospital admission, but statistics for patients treated for CAP in the ambulatory setting are difficult to obtain. Overall, incidence of CAP in 1994 was 170 cases per 10,000 individuals.

International

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 are highest in elderly patients.

Race

All races are affected equally.

Sex

No sex-related differences exist.

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

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History

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

• Typically, patients with bacterial CAP present with variable degrees of fever, usually with a productive cough and often with pleuritic chest pain.
• Clinical presentation in patients with CAP due to atypical pathogens usually is less acute than in those with 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 infections 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 infections, chest pain usually is not a feature of nonzoonotic atypical pathogens causing CAP.

Physical

• With typical bacterial CAP, abnormal physical findings are confined to the chest.
• 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.
• Patients with pleural effusion (usually due to Haemophilus influenzae) have signs of pleural effusion if it is large enough to be detected during the physical examination.
• Patients with pleural effusion have decreased tactile fremitus and dullness upon chest percussion.
• Purulent sputum is characteristic of pneumonia caused by typical bacterial pathogens and usually is not a feature of atypical pathogens, with the exception of Legionnaires disease.
• Blood-tinged sputum may be found 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.
• Pleural effusion in a patient with CAP and extrapulmonary manifestations should suggest the presence of Legionella species. Pleural effusion with an appropriate epidemiologic history, such as contact with a rabbit or deer, may suggest the presence of tularemia.
• Patients presenting with acute heart failure, such as acute myocardial infarction without preexisting congestive heart failure (CHF), often have normal cardiac silhouettes, bilateral symmetric moist rales, and an S3 gallop rhythm present upon auscultation.
• Severe CAP is caused by the same spectrum of pathogens as mild or moderately severe CAP.
• • Severity of CAP is determined by the preexisting function of the heart, lungs, and spleen.
  • Host factors, not different or more virulent pathogens, make CAP mild or severe.

Causes

Table 1. Respiratory Pathogens and Nonpathogens in Community-Acquired Pneumonia

Typical Bacterial Pathogens in CAP (approximately 85%) Streptococcus pneumoniae Penicillin-sensitive S pneumoniae Penicillin-resistant S pneumoniae H influenzae Ampicillin-sensitive H influenzae Ampicillin-resistant H influenzae Moraxella catarrhalis (all strains penicillin resistant) Atypical Respiratory Pathogens in CAP (approximately 15%) Legionella species Mycoplasma species C pneumoniae Rare Bacterial Pathogens in CAP Klebsiella pneumoniae - Only in those with chronic alcoholism Staphylococcus aureus - Postviral influenza setting Pseudomonas aeruginosa - Only in patients with cystic fibrosis or bronchiectasis Nonpulmonary Pathogens in Pneumonia Nonaeruginosa pseudomonads Stenotrophomonas (Xanthomonas) maltophilia Citrobacter freundii Burkholderia (Pseudomonas) cepacia Citrobacter koseri Enterobacter species Flavobacterium species Enterobacter cloacae Flavobacterium meningisepticum Enterobacter agglomerans Enterococcus species

Adapted with permission from Cunha BA:
Severe community-acquired pneumonia. Crit Care Clin 1998;14:105-118

• Typical bacterial pathogens
• • Typical bacterial pathogens causing CAP are S pneumoniae (see Image 1), H influenzae (see Image 2), and M catarrhalis (see Image 3).
  • • In patients with chronic bronchitis who develop CAP requiring hospitalization, M catarrhalis is particularly common.
    • S pneumoniae remains the most common agent responsible for CAP.
  • Importantly, S aureus, K pneumoniae, and P aeruginosa are not causes of CAP in typical hosts.
  • • S aureus causes CAP in the setting of postviral influenza.
    • K pneumoniae 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 certainly occur, but they 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 causing 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.
    • The appropriate epidemiologic questions for patients with Q fever include recent close contact with a parturient cat or sheep.
    • Patients who are suspected of having psittacosis have a history of recent close contact with psittacine birds.
    • Patients with tularemia have a history of recent close contact with deer or rabbits or recently have been bitten by a tick or deer fly.
  • Nonzoonotic atypical pneumonias are caused by Legionella species, M pneumoniae, or C pneumoniae.
  • The pattern of extrapulmonary findings, not individual findings, allows the clinician to differentiate between typical and atypical pneumonias.
  • Typical bacterial pneumonias have few, if any, extrapulmonary findings. Each atypical pathogen has its own distribution pattern of extrapulmonary organ involvement, which permits an accurate and rapid presumptive clinical diagnosis (see Image 4).

    Table 2. Differential Diagnostic Features of the Atypical Pneumonias
    
    

    	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)	±

    Adapted from: Cunha BA. Clinical features of Legionnaires disease. Semin Respir Infect 1998; 13:116-127.

  • Legionella species are the most important atypical pathogen causing CAP.
  • Although Q fever and psittacosis are associated with relative bradycardia, these zoonotic pneumonias may be excluded by a negative epidemiologic vector contact history.
  • If psittacosis and Q fever are eliminated from the diagnostic consideration by history, then 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).
    • 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 4).
  • Table 3. Relative Bradycardia

    Determination and Evaluation of Relative Bradycardia
    Inclusive criteria	Patient must be an adult, ie, >12 y
    	Patient must have a temperature >101°F
    	Pulse must be taken simultaneously with the temperature elevation
    Exclusive criteria	Patient has normal sinus rhythm without arrhythmia, second-degree/third-degree heart block, or pacemaker-induced rhythm
    	Patient must not be on beta-blocker medication
    Appropriate Temperature-Pulse Relationships (temperature and corresponding pulse [beats/min])
    41.1°C/106°F = 150/min 40.6°C/105°F = 140/min 40.0°C/104°F = 130/min 39.5°C/103°F = 120/min 38.9°C/102°F = 110/min
    Causes of Relative Bradycardia
    Infectious causes	Legionella species 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 is the lack of response to beta-lactam antibiotic treatment in a patient with CAP and relative bradycardia. If other causes of relative bradycardia are excluded, this is a clue because it is a constant early finding in Legionnaires disease.

    Table 4. Modified Winthrop University Hospital Infectious Disease Division's Point System for Diagnosing Legionnaires Disease in Adults
    
    

    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 radiograph	Rapidly progressive asymmetrical infiltrates* (excluding severe influenza/SARS)	+3
    ↓ PO 2 with ↑ A-a gradient (> 35)*	(Excluding severe influenza/SARS)	-5
    ↓ Na +	Acute onset	+1
    ↓ PO 4 =*	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
    Total Points	>15, Legionella very likely
    	5-15, Legionella likely
    	<5 Legionella unlikely

    * Otherwise unexplained (acute and associated with pneumonia)

    Adapted from: Cunha BA. Pneumonia Essentials. Physicians Press; 2006.
    

  • In typical hosts, CAP does not present with shock. If CAP presents with shock, look for impaired or absent splenic function. Disorders associated with impaired splenic function include those listed in Table 5.

    Table 5. Differential Diagnosis of Severe Community-Acquired Pneumonia Presenting With Shock
    

    Chronic alcoholism Amyloidosis Chronic active hepatitis Fanconi syndrome Hyposplenism of 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

    Adapted with permission from:
    Cunha BA. Strategies for managing severe community-acquired pneumonia. J Crit Illness 1997:12:711-721
    

  • • If CAP presents with shock in the absence of conditions associated with hyposplenism, look for mimics of pneumonia that present with pulmonary infiltrates on chest films, fever, leukocytosis, and hypotension, such as acute myocardial infarction or acute pulmonary embolism.
    • If CAP presents with shock and without evidence of hyposplenia, acute myocardial infarction, or acute pulmonary embolism, consider an exacerbation of preexisting cardiopulmonary disease that presents with hypotension and coronary insufficiency with hypoxemia or emphysema.

DIFFERENTIALS

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Other Problems to be Considered

Congestive Heart Failure and Pulmonary Edema
Asthma
Fever secondary to community-acquired pneumonia (CAP) may precipitate a myocardial infarction
Tracheobronchitis
SLE pneumonitis
Acute drug hypersensitivity reactions (nitrofurantoin)
Pulmonary embolus or infarction
Bronchogenic carcinoma

WORKUP

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Lab Studies

• Send the sputum of patients with community-acquired pneumonia (CAP) for a Gram stain and/or culture. Many patients, especially elderly patients, may not be able to produce an adequate suitable sputum sample.
• • Patients with Legionnaires disease and purulent sputum show few or no predominant organisms after the Gram stain.
  • 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, frequently are associated with positive blood cultures. M catarrhalis bacteremia is unusual.
• Presentation with CAP and extrapulmonary findings is suggestive of the presence of 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 pneumonia caused by Legionella species.
  • 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 a variety of viral and neoplastic illnesses. In patients with Mycoplasma-associated pneumonia, 75% develop transient elevations of cold agglutinins early in the course of the illness.
• • A negative cold agglutinin titer does not exclude the presence of Mycoplasma species.
  • A moderately elevated cold agglutinin titer effectively rules out Legionella pneumonia. Because low titer elevations of cold agglutinins are not specific, 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 is (>1:64), the more likely the cold agglutinins are due to Mycoplasma species.
• If a patient is suspected of having Legionella pneumonia, direct fluorescent antibody (DFA) testing of the sputum can assist in making the diagnosis if obtained early and before antimicrobial treatment. Antimicrobial treatment rapidly decreases the sputum yield of DFA testing (see Image 5).
• Send serology if zoonotic atypical pathogens are suspected because isolation and culture are difficult and dangerous for microbiology personnel. A diagnosis of zoonotic pathogen-associated pneumonia is based on a 4-fold or greater increase in titers between acute and convalescent serum specimens.
• Order 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 the diagnosis of acute infection. An increase in the IgM titer for either pathogen allows the clinician to make the diagnosis in a patient with CAP.
• Order Legionella serologies if Legionella pneumonia is suggested based on the pattern of extrapulmonary findings. If acute titers are negative, this does 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 titers.
• The Legionella urine antigen test is only applicable for the Legionella pneumophila serogroup type I, which accounts for approximately 80% of infections. The urinary antigen test for Legionella species infections remains positive for long periods but may be negative early in the infection.
• If C pneumoniae is suspected, order specific pneumonia IgM and IgG titers. Do not order chlamydial titers without specifying the species.
• Approach CAP in patients with HIV as follows:
• • The pathogen causing CAP in patients with HIV is determined by the CD4 count. The differential diagnosis of the pathogen is determined by assessing the CD4 count and the chest x-ray appearance in the patient with HIV (see Image 8).
  • Patients with HIV and normal or slight decreases in their CD4 count with focal infiltrates have approximately the same pathogen distribution as typical hosts. Patients with nonfocal infiltrates or hypoxemia may have Pneumocystis carinii pneumonia when the CD4 count is decreased appropriately.
  • Patients with HIV, 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).

Imaging Studies

• Order a chest x-ray in all patients suspected of having CAP.
• • Obtain a chest x-ray 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 x-ray. In these patients, repeat the chest x-ray within 24 hours.
  • Chest x-ray assists with the differentiation of viral pneumonias from nonviral pneumonias. Viral pneumonias have few or no infiltrates on chest x-ray, but, when present, infiltrates almost always are 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 x-ray, with or without consolidation or pleural effusion.
  • Chest x-ray findings should be negative in patients with asthma who do not have CAP. Chest x-ray findings also are negative in patients with chronic bronchitis.
  • The infiltrates observed with CHF appear as increased interstitial markings and vascular redistribution to the upper lobes. Usually, cardiomegaly is present in patients with preexisting heart failure.
  • Rapid cavitation is not a usual 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. Findings of cavitation are not present on the initial chest x-ray in patients with CAP due to aspiration.
• Serial chest x-rays can be used to observe the progression of CAP.
• • Rapidly progressive asymmetric infiltrates suggest the possibility of Legionnaires disease.
  • The appearance of chest x-ray findings worsens over a short period and requires a long time 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 exist that are not consistent with the diagnosis of pneumonia only.

Procedures

• 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 by other available diagnostic measures. This procedure is most useful to assess 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

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Medical Care

Table 6. Empiric Therapeutic Approach to Community-Acquired Pneumonia in Patients With HIV

CAP with the Following: Chest x-ray: Focal infiltrate CD4: ³200 cells/mm3	CAP with the Following: Chest x-ray: Focal infiltrate CD4: Very low (£200 cells/mm3)
Most Likely Pathogen S pneumoniae H influenzae M legionella Salmonella C pneumoniae	Most Likely Pathogen Those causing tuberculosis Mycobacterium avium-intracellulare
Optimal Empiric Therapy Extrapulmonary findings (atypical pathogens): Respiratory quinolone or Doxycycline No Extrapulmonary findings (typical bacteria): Ceftriaxone or Third-generation cephalosporins or Cefepime or Respiratory quinolone Features of both typical and atypical: Respiratory quinolone Doxycycline Telithromycin	Optimal Empiric Therapy Tuberculosis: Isoniazid, ethambutol, rifampin, pyrazinamide Mycobacterium avium-intracellulare: Azithromycin + Ethambutol ± Rifampin or Azithromycin + Ethambutol + Levofloxacin

• Hospitalize patients with community-acquired pneumonia (CAP) who are moderately to severely ill. Factors that predict risk for increased mortality in patients with CAP have been studied and include older age, significant comorbidities, increased respiratory rate, hypotension, fever, multilobar involvement, anemia, and hypoxia, to name a few.
• 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 treating the patient with antibiotics for CAP.
• Patients admitted with severe CAP and hypotension or shock often are 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 preexisting CHF), the patient with shock likely has diminished or absent splenic function.
• • Many underlying conditions are associated with diminished splenic function that may present as severe CAP.
  • An abdominal scar resulting from abdominal trauma or lymphoma staging is an obvious manifestation of possible asplenia.
  • Investigate for the disorders associated with hyposplenic function as indicated in Table 5.
  • Hyposplenism may be inferred from the presence of Howell-Jolly bodies in the peripheral blood smear in a patient presenting with CAP who is in shock. The first step in treating a patient in shock is effective intravascular volume replacement. If aggressive intravascular replacement is inadequate, then pressors may be added. Do not administer pressors before adequate volume replacement because effective intracirculating intravascular volume decreases and the blood pressure drops further.
• Treatment of penicillin-resistant pneumococcal pneumonia is as follows:
• • The overuse of beta-lactam and macrolide antibiotics probably has caused a gradual increase in the S pneumoniae minimal inhibitory concentration (MIC). This relative increase in the MIC (ie, intermediate resistance or relative resistance) can be overcome by using full recommended doses of beta-lactams.
  • In most cases of penicillin-resistant S pneumoniae, treatment remains penicillin. Most strains have increased MICs but still are susceptible and are not clinically resistant to penicillin.
  • Penicillin resistance is classified according to MICs. Breakpoints are as follows:
  • • Sensitive - Equal to or less than 0.6 mcg/mL
    • Intermediate resistance - 0.1-1 mcg/mL
    • Highly resistant - Equal to or greater than 2 mcg/mL (fortunately, few highly penicillin-resistant pneumococci exist)
  • 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, should decrease penicillin resistance among pneumococci.
  • The widespread use of macrolides, such as trimethoprim-sulfamethoxazole (TMP-SMX) and tetracycline (excluding doxycycline), has been associated with H influenzae resistance.
  • Most oral cephalosporins, except cefprozil, have been associated with increased S pneumoniae resistance.
  • Worldwide, the unrestricted use of levofloxacin since 1993 has not resulted in any increase in S pneumoniae resistance, although one study in Canada demonstrated an increase in fluoroquinolone resistance in its pneumococcal isolates from 1993-1998.
• Use of intravenous-to-oral switch programs is as follows:
• • Most patients admitted to the hospital with CAP 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, patients may be switched to equivalent oral therapy to complete a 2-week course of therapy after 48 hours.
  • Candidate agents for intravenous-to-oral (IV-to-PO) switch programs have the same spectrum as intravenous agents, excellent bioavailability, few adverse effects, low resistance potential, and relatively low cost. Ideal agents for IV-to-PO switch programs include levofloxacin and doxycycline.
• • Other agents that may be used if S pneumoniae is not the etiologic agent include azithromycin or clarithromycin.

    Table 7. Community-Acquired Pneumonia: Therapeutic Principles
    

    Pathogens Single pathogens cause CAP. Multiple pathogens rarely, if ever, cause CAP. Rarely, if ever, is CAP caused by more than 1 typical or 2 atypical organisms or multiple typical/atypical organisms. Studies describing 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 multiple-drug therapy. The addition and/or change of antibiotics because of severity of illness and/or comorbidities is not rational. Antimicrobial therapy is directed against the pathogen, not against the comorbid factors. Comorbidity is an important prognostic factor and contributes to the severity index, but it 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 presenting 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 usual 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 No need exists to cover S aureus, Klebsiella species, or P aeruginosa in CAP (most CAP regimens include K pneumoniae coverage). No need exists to cover oral anaerobes in community-acquired aspiration pneumonia. Virtually all antibiotics used to treat community-acquired aspiration pneumonia are highly effective against oral anaerobes. B fragilis coverage with metronidazole or clindamycin is unnecessary. Coverage should include the typical (S pneumoniae, H influenzae, M catarrhalis) and atypical (Legionella and Mycoplasma species, C pneumoniae) pathogens. Nursing home-acquired pneumonia (NHAP) should be treated as CAP. NHAP pathogens most closely resemble CAP and not hospital-acquired pathogens, eg, P aeruginosa. Therapeutic considerations Monotherapy coverage of both typical and atypical pathogens in CAP is preferred to double-drug therapy. Monotherapy is less expensive and as effective as double-drug regimens. Avoid empiric macrolide monotherapy because approximately 25% of S pneumoniae are naturally resistant to all macrolides. Preferred monotherapy for CAP includes doxycycline, telithromycin, or respiratory quinolones. 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 PO/IV forms. It is ideal for IV-to-PO switch monotherapy from patient compliance, safety, and cost perspectives. In patients with CAP who are able to take PO medication, switch from IV to PO after 48 hours, using an antibiotic with the appropriate spectrum, high bioavailability, few adverse gastrointestinal effects, little or no resistance potential, and relatively low cost such as doxycycline, respiratory quinolones, or telithromycin. Penicillin-resistant S pneumoniae Most penicillin resistance is "relative resistance" and is readily treatable with penicillin and/or beta-lactams. Most highly penicillin-resistant S pneumoniae (MIC >2 mcg/mL) also may be treated with beta-lactams. Alternately, doxycycline, telithromycin, or respiratory quinolones may be used. Vancomycin rarely, if ever, is needed. Very highly penicillin-resistant S pneumoniae (MIC 6 mcg/mL) remains a rare cause of CAP.

    Table 8. Empiric Therapy of Hospitalized Patients With Community-Acquired Pneumonia
    

    Suboptimal regimens Monotherapy Ceftriaxone Covers typical pathogens, misses atypical pathogens Adverse effects - Diarrhea not caused by C difficile, pseudobiliary lithiasis Moderately expensive 1 g (IV) q24h $27 (antibiotic cost) + $10 (IV charge) = $37/d (cost to institution) Azithromycin Misses approximately 25% of S pneumoniae, should not be used alone, covers atypical pathogens Adverse effects - Nausea, vomiting, diarrhea not caused by C difficile Very low serum levels - Slow onset/delayed therapeutic effect Moderately expensive - $20 (antibiotic cost) + $10 (IV charge) = $30/d (cost to institution) Combination therapy Ceftriaxone plus erythromycin - Most expensive regimen Covers typical and atypical organisms Adverse effects - Nausea, vomiting, diarrhea not caused by C difficile, phlebitis, cardiac effects (QTc), pseudobiliary lithiasis Most expensive combination Ceftriaxone 1 g IV q24h = $37/d plus erythromycin 1 g IV q6h = $50/d Total cost = $87/d (cost to institution) IV-to-PO switch therapy - Disadvantage of double-drug therapy (relatively expensive/inconvenient) Ceftriaxone plus azithromycin - Very expensive regimen Covers typical and atypical pathogens Adverse effects - Nausea, vomiting, diarrhea not caused by C difficile, phlebitis, cardiac effects (QTc), pseudobiliary lithiasis Ceftriaxone 1 g IV q24h = $37/d plus azithromycin 500 mg IV q24h = $30/d Total cost = $67/d (cost to institution) IV-to-PO switch therapy - Disadvantage of double-drug therapy (relatively expensive/inconvenient) Optimal regimens Monotherapy Respiratory quinolones Levofloxacin Moxifloxacin Gatifloxacin Telithromycin Doxycycline

Consultations

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

Diet

Diet is as tolerated.

Activity

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

MEDICATION

Section 7 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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 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 differentiate typical and atypical pneumonias on clinical grounds, combination therapy with a beta-lactam, such as ceftriaxone, in addition to erythromycin to cover both typical and atypical pathogens, became popular.

Even though 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.

Severity of CAP determines the route of antibiotic administration (ie, PO for mild cases, IV 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 is the same, regardless of severity.

Because the severity of CAP is determined by impaired 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 not logical. Antimicrobial therapy is directed against the microorganism and does not improve cardiopulmonary or splenic function, regardless of the degree of severity.

Drug Category: Antibiotics

Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.

Drug Name	Gemifloxacin (Factive)
Description	Fluoroquinolone antibiotic with wide range of activity against gram-negative and gram-positive organisms. Acts by inhibiting both DNA gyrase and topoisomerase IV (TOPO IV), which are essential for bacterial growth. Because of this dual mechanism, MIC values remain in the susceptible range for some double mutants (eg, Streptococcus pneumoniae). Indicated for mild-to-moderate CAP caused by S pneumoniae (including penicillin-resistant strains; MIC value for penicillin > 2 mg/mL), Haemophilus influenzae, Moraxella catarrhalis, Mycoplasma pneumoniae, Chlamydia pneumoniae, or Klebsiella pneumoniae.
Adult Dose	CAP due to known or suspected S pneumoniae, H influenzae, M pneumoniae, or C pneumoniae: 320 mg PO qd for 5 d CAP due to known or suspected K pneumoniae, M catarrhalis, or multidrug-resistant S pneumoniae: 320 mg PO qd for 7 d
Pediatric Dose	<18 years: Not established >18 years: Administer as in adults
Contraindications	Documented hypersensitivity to gemifloxacin or other fluoroquinolones
Interactions	Coadministration with antacids and divalent or trivalent cations (eg, aluminum, magnesium, iron) significantly reduces absorption (administer 3 h before or 2 h after gemifloxacin); sucralfate decreases absorption and should be administered 2 h following gemifloxacin; may increase QT interval prolongation risk if coadministered with class IA (eg, quinidine, procainamide) or class III antiarrhythmic agents (sotalol, amiodarone), or other drugs known to prolong QT interval (eg, erythromycin, antipsychotics, antidepressants)
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Decrease dose by 50% with CrCl <40 mL/min; may prolong QT interval; may cause maculopapular rash

Drug Name	Ceftriaxone (Rocephin)
Description	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.
Adult Dose	2 g IV q12-24h; not to exceed 4 g/d
Pediatric Dose	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
Contraindications	Documented hypersensitivity
Interactions	Probenecid may decrease clearance, causing an increase in ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
Pregnancy	B - Usually safe but benefits must outweigh the risks.
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

Drug Name	Azithromycin (Zithromax)
Description	Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing arrest of RNA-dependent protein synthesis.
Adult Dose	500 mg IV q24h for 3 d, then 500 mg/d PO for 7-10 d
Pediatric Dose	<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
Contraindications	Documented hypersensitivity; hepatic impairment; do not administer with pimozide
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
Pregnancy	B - Usually safe but benefits must outweigh the risks.
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

Drug Name	Doxycycline (Vibramycin)
Description	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.
Adult Dose	100-200 mg PO/IV q12h
Pediatric Dose	<8 years: Not recommended >8 years: 2-5 mg/kg/d PO/IV in 1-2 divided doses; not to exceed 200 mg/d
Contraindications	Documented hypersensitivity; avoid in pregnancy and children <8 y
Interactions	Bioavailability minimally decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate
Pregnancy	D - Unsafe in pregnancy
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

Drug Name	Telithromycin (KETEK)
Description	First antibiotic in a new class called ketolides. Blocks protein synthesis by binding to 50S ribosomal subunit (23S rRNA at domain II and V). Binding at domain II retains activity against gram-positive cocci (eg, S pneumoniae) in the presence of resistance. Resistance and cross-resistance have not been observed. Indicated to treat mild-to-moderate CAP, including infections caused by multidrug-resistant S pneumoniae.
Adult Dose	800 mg PO qd for 7-10 d
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; coadministration with cisapride or pimozide; myasthenia gravis; history of hepatitis and/or jaundice with use of macrolides
Interactions	CYP 3A4 inhibitor and substrate; coadministration with other CYP 3A4 inhibitors (eg, itraconazole, ketoconazole) decreases elimination and increases Cmax and AUC; CYP 3A4 inducers (eg, rifampin) decreases telithromycin Cmax and AUC by 79% and 86% respectively; increases Cmax and AUC of other CYP 3A4 substrates (eg, cisapride, pimozide, simvastatin, lovastatin, atorvastatin, midazolam, triazolam); HMG-CoA reductase inhibitors (eg, simvastatin, atorvastatin, lovastatin) should be temporarily discontinued owing to increased myopathy risk when coadministered; increases digoxin and theophylline serum levels; decreases sotalol Cmax and AUC secondary to decreased absorption; caution with other drugs that increase QTc interval (eg, quinidine, procainamide, dofetilide)
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in severe renal impairment (limited data exist); consider the diagnosis of pseudomembranous colitis if diarrhea occurs following antibiotic treatment; may prolong QTc interval, caution with heart conduction abnormalities; common adverse effects include diarrhea and nausea; may rarely cause visual disturbances or increased liver enzyme levels; acute hepatic failure and severe liver injury (in some cases fatal) have been reported (if clinical hepatitis or liver enzyme elevations combined with other systemic symptoms occur, permanently discontinue)

Drug Name	Moxifloxacin (Avelox)
Description	Inhibits the A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription. Indicated for CAP, including multidrug-resistant S pneumoniae.
Adult Dose	400 mg PO/IV qd
Pediatric Dose	<18 years: Not recommended >18 years: Administer as in adults
Contraindications	Documented hypersensitivity; known Q-T prolongation, concurrent administration of drugs that cause Q-T prolongation
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
Pregnancy	C - Safety for use during pregnancy has not been established.
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

Drug Name	Gatifloxacin (Tequin)
Description	Quinolone that has antimicrobial activity based on ability to inhibit bacterial DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. Quinolones have broad activity against gram-positive and gram-negative aerobic organisms. Differences in chemical structure between quinolones have resulted in altered levels of activity against different bacteria. Altered chemistry in quinolones result in toxicity differences.
Adult Dose	200-400 mg PO/IV qd
Pediatric Dose	<18 years: Not recommended >18 years: Administer as in adults
Contraindications	Documented hypersensitivity
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; may reduce therapeutic effects of phenytoin; probenecid may increase serum concentrations of quinolones May increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Quinolones increase risk of pseudomembranous colitis caused by Clostridium difficile; may cause severe photosensitivity reactions in patients exposed to sunlight or UV light; have been associated with various CNS manifestations such as hallucinations and seizures; factors that increase risk of adverse effects should be noted when considering use of any quinolone; caution in renal insufficiency (adjust dose)

Drug Name	Ertapenem (Invanz)
Description	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.
Adult Dose	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 Dose	<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
Contraindications	Documented hypersensitivity to drug or amide-type anesthetics
Interactions	Probenecid may reduce renal clearance of ertapenem and increase half-life but benefit is minimum and does not justify coadministration
Pregnancy	B - Usually safe but benefits must outweigh the risks.
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

Drug Name	Amoxicillin and clavulanate (Augmentin, Augmentin XR)
Description	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.
Adult Dose	Extended-release: Amoxicillin 2 g/clavulanate 125 mg (ie, 2 extended-release tabs) PO q12h for 7-10 d
Pediatric Dose	<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
Contraindications	Documented hypersensitivity
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
Pregnancy	B - Usually safe but benefits must outweigh the risks.
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

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Patients with 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 community-acquired pneumonia (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 x-ray is advisable. As long as the patient is improving and parapneumonic complications are not evident, a posttherapy chest x-ray is not needed.

In/Out Patient Meds

• Most patients with CAP who are admitted to the hospital are treated intravenously for 2 days and then complete a 12-day 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 medications administered orally 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 as an inpatient or an outpatient. Patients receiving oral antibiotics may be admitted for hospital services, such as pulmonary toilet and additional diagnostic tests, that are not obtainable on an outpatient basis.
• If patients are switched to an oral regimen and are 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 of time. Patients who are debilitated (eg, those with underlying disorders, compromised hosts) may require longer periods of treatment that are based on clinical response.
• IV-to-PO switch therapy is optimal with 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, therefore, may remain susceptible to pneumococcal pneumonia. The same is true concerning the use of the Haemophilus vaccine.

Complications

• Infections caused by S pneumoniae may be complicated by a 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.
• Infections caused by K pneumoniae, occurring only in patients with chronic alcoholism, also may be complicated by empyema. Cavitation from Klebsiella species 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 with H influenzae is part of the disease process and should not be viewed as a complication.
• M catarrhalis usually is not associated with bacteremia, pleural effusions, or empyema; however, M catarrhalis causing CAP in a patient with advanced lung disease may prove fatal because of the underlying pulmonary condition of the host.
• Consider extrapulmonary manifestations associated with M pneumoniae as part of the disease process and not as complications. Following an infection with M pneumoniae, patients may develop short-term or permanent asthma.
• As with Mycoplasma-associated pneumonia, Chlamydia-associated 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

• 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, patients who are older do not fare as well as younger adults.
• Patients with impaired splenic function may develop overwhelming pneumococcal sepsis and experience a fatal outcome in 12-24 hours, regardless of the antimicrobial regimen used.
• Prognostic factors that predict a bad outcome include preexisting lung disease, underlying cardiac disease, advanced age, multilobar involvement, and delay in the initiation of appropriate antimicrobial therapy.

Patient Education

• Remind patients 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

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Be wary if patients present 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. Also, if a cardiopulmonary reason for the severity of CAP or hypotension is not apparent, 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 patients who are pregnant and 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 for patients in the pediatric age group, excluding the very young (ie, <6 y).
• When diagnosing CAP, first exclude other pulmonary conditions that may mimic the clinical presentation of CAP.
• • New onset of CHF or an exacerbation of preexisting CHF may result in cough or shortness of breath, which commonly is confused with CAP.
  • Fever secondary 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 initially may be confused with CAP; however, in patients with bronchitis, the chest x-ray should reveal no infiltrates in the presence of bronchitis.
  • Various other noninfectious disorders occasionally may mimic CAP, such as SLE pneumonitis, acute drug hypersensitivity reactions (nitrofurantoin), and pulmonary embolus or infarction.
  • Bronchogenic carcinoma may mimic CAP. Bronchiogenic carcinoma also may predispose patients 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 x-ray readily helps differentiate asthma from CAP because no infiltrates are present on the chest x-ray in asthma.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Gram stain showing Streptococcus pneumoniae.
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Media type:  Photo