Bacterial Pneumonia Treatment & Management

  • Author: Nader Kamangar, MD, FACP, FCCP, FCCM; Chief Editor: Zab Mosenifar, MD   more...
 
Updated: Jan 3, 2012
 

Approach Considerations

Almost all major decisions regarding management of pneumonia address the initial assessment of severity. See Risk Stratification under Clinical Presentation.

Perhaps the most important initial determination is that of the need for hospitalization. In determining site or level of care, options include outpatient, medical ward care, or medical intensive care unit (ICU) management.

Consider using the pneumonia severity index (PSI) score as a guide for inpatient care and mortality risk. The Agency for Healthcare Research and Quality (AHRQ) has an interactive tool to calculate the PSI score.[34]

Note that the PSI score may underestimate the patient's need for admission (ie, a young otherwise healthy patient who is vomiting or has social factors that precludes him or her taking medicine). Conversely, the PSI score tends to overestimate the mortality in the higher risk patients.

Direct admission to an intensive care unit (ICU) is mandated for any patient in septic shock with a requirement for vasopressors or with acute respiratory failure requiring intubation and mechanical ventilation.

Transfer, if needed, is safe for a patient in otherwise stable condition who is being admitted for antibiotic therapy and pulmonary toilet. Patients who are severely ill and those with signs of respiratory failure, sepsis, and/or neutropenia must be stabilized before transfer.

Respiratory support

Antibiotic therapy is the mainstay of treatment of bacterial pneumonia. However, patients who have bronchospasm with infection benefit from inhaled bronchodilators, administered by means of a nebulizer metered-dose inhaler.

For patients with mild shortness of breath, only supplemental oxygen with a nasal cannula may be required for ventilatory support. Administer ventilatory support when simple supplemental oxygen is not sufficient or when the patient cannot cope with the work of breathing.

Moderate dyspnea requires high oxygen concentrations, such as those provided by a Venti-mask or partial rebreathing face mask. Use these masks with caution in patients with chronic obstructive pulmonary disease (COPD). Patients in respiratory failure or those with COPD who need high oxygen concentrations may require endotracheal intubation and ventilation.

An alternative to intubation may be use of a continuous positive airway pressure (CPAP) mask. Patients who are awake and can tolerate mask application may avoid intubation. However, in patients with productive cough, noninvasive ventilation is often avoided because it may impair clearance of respiratory secretions, which can lead to worsening infection and recurrent aspiration. Nasal CPAP is not usually as well tolerated as a full mask (which covers both the nose and mouth) in the emergent situation.

Fluid resuscitation

Patients with hypotension and/or tachycardia may benefit from an intravenous crystalloid bolus in the field. Many individuals with pneumonia also have volume depletion. In elderly patients with underlying cardiac disease, take care to avoid aggressive fluid administration, which may cause volume overload.

Empiric antibiotic therapy

Empiric therapy for the hospitalized patient should be initially broad and cover the likely causative organisms. Use caution in patients who are elderly or debilitated. If bacteremia is present in persons with pneumococcus who are older than 80 years, the mortality rate remains approximately 40%, even with treatment.

Many regions have guidelines for evaluation and treatment of community-acquired pneumonia (CAP). This usually includes a minimum time from door to antibiotic of 4 hours or less. Failure to abide by these time parameters may be associated with poor outcome. When in doubt, administer the first antibiotic dose.

Other initial treatments may include correction of electrolyte levels and chest physiotherapy (to assist in drainage of secretions).

See Antimicrobial Therapy.

Corticosteroids

The role of supplementing corticosteroids in patients with hypotension from septic shock remains controversial. Previously, it was recommended that septic patients who were hypotensive despite fluid resuscitation and vasopressor support be screened for occult adrenal insufficiency. However, current guidelines recommend empiric therapy with stress-dose steroids in these patients who remain hypotensive despite fluids and pressors, to avoid delay in treatment of presumed adrenal insufficiency.[57]

Drotrecogin alfa

A recombinant version of human activated protein C, drotrecogin alfa (Xigris) is the first immunomodulatory drug approved for the treatment of severe sepsis. It is recommended in patients with CAP who have persistent septic shock despite adequate fluid resuscitation. Its use is recommended in patients at high risk of death.

Drotrecogin alfa was withdrawn from the worldwide market October 25, 2011 after analysis of the Recombinant Human Activated Protein C Worldwide Evaluation in Severe Sepsis (PROWESS)-SHOCK clinical trial. Drotrecogin alfa failed to demonstrate a statistically significant reduction in 28-day all-cause mortality in patients with severe sepsis and septic shock. Trial results observed a 28-day all-cause mortality rate of 26.4% in patients treated with activated drotrecogin alfa compared with 24.2% in the placebo group of the study.

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Antimicrobial Therapy

The goals of pharmacotherapy for bacteria pneumonia are to eradicate the infection, reduce morbidity, and prevent complications.

Treatment of pneumonia depends largely on the empiric use of antibiotic regimens directed against potential pathogens as determined by the setting in which the infection took place and the potential for exposure to multidrug-resistant (MDR) organisms and other more virulent pathogens (ie, community-acquired pneumonia [CAP], healthcare-acquired pneumonia [HCAP], hospital-acquired pneumonia [HAP], ventilator-associated pneumonia [VAP]). Discussion of empiric antibiotic therapy can be based on hospitalization status.

The information in this section is derived mainly from the current Infectious Diseases Society of America/American Thoracic Society (IDSA/ATS) guidelines for the management of CAP.[16] These guidelines have been assessed in research studies since their release, with evidence of improved health outcomes, decreased length of hospital stay, and overall decreased mortality in patients hospitalized with CAP.[58, 59]

As discussed earlier, initial empiric therapy for hospitalized patients should be broad and cover the likely causative organisms. Direct the use of antibiotic agents in bacterial pneumonia based on laboratory data as well as clinical response.

The possibility of Legionella infection should always be considered when evaluating CAP, because delayed treatment significantly increases mortality. The most prevalent causative organism is S pneumoniae, regardless of the host or the setting; empiric therapy must be selected with this consideration in mind.

Antibiotics and HAP and VAP

The prevalence and resistance patterns of MDR pathogens vary between institutions and even between ICUs within the same institution; therefore, appropriate initial antibiotic therapy for HAP and VAP may vary markedly according to hospital site. Antimicrobial prescribing practices should not necessarily be based on national guidelines, but rather on patterns of MDR organisms at individual institutions.[5]

The table below presents first- and second-line antibiotic choices for specific organisms that cause bacterial pneumonia.

Table. Pathogen-Driven Antibiotic Choices[16] (Open Table in a new window)

OrganismFirst-Line AntimicrobialsAlternative Antimicrobials
Streptococcus pneumoniae
Penicillin susceptible



(MIC < 2 mcg/mL)



Penicillin G, amoxicillinMacrolide, cephalosporin (oral or parenteral), clindamycin, doxycycline, respiratory fluoroquinolone
Penicillin resistant



(MIC ≥2 mcg/mL)



Agents chosen on the basis of sensitivityVancomycin, linezolid, high-dose amoxicillin (3 g/d with MIC ≤4 mcg/mL
Staphylococcus aureus
Methicillin susceptibleAntistaphylococcal penicillinCefazolin, clindamycin
Methicillin resistantVancomycin, linezolidTrimethoprim- sulfamethoxazole
Haemophilus influenzae
Non–beta-lactamase producingAmoxicillinFluoroquinolone, doxycycline, azithromycin, clarithromycin
Beta-lactamase producingSecond- or third-generation cephalosporin, amoxicillin/clavulanateFluoroquinolone, doxycycline, azithromycin, clarithromycin
Mycoplasma pneumoniaeMacrolide, tetracyclineFluoroquinolone
Chlamydophila pneumoniaeMacrolide, tetracyclineFluoroquinolone
Legionella speciesFluoroquinolone, azithromycinDoxycycline
Chlamydophila psittaciTetracyclineMacrolide
Coxiella burnetiiTetracyclineMacrolide
Francisella tularensisDoxycyclineGentamicin, streptomycin
Yersinia pestisStreptomycin, gentamicinDoxycycline, fluoroquinolone
Bacillus anthracis (inhalational)Ciprofloxacin, levofloxacin, doxycyclineOther fluoroquinolones, beta-lactam (if susceptible), rifampin, clindamycin, chloramphenicol
EnterobacteriaceaeThird-generation cephalosporin, carbapenemBeta-lactam/beta-lactamase inhibitor, fluoroquinolone
Pseudomonas aeruginosaAntipseudomonal beta-lactam plus ciprofloxacin, levofloxacin, or aminoglycosideAminoglycoside plus ciprofloxacin or levofloxacin
Bordetella pertussisMacrolideTrimethoprim- sulfamethoxazole
Anaerobe (aspiration)Beta-lactam/beta-lactamase inhibitor, clindamycinCarbapenem
MIC = Minimal inhibitory concentration.
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Outpatient Empiric Antibiotic Therapy

Antibiotic choices in the outpatient setting should be driven by the presence of patient risk factors, including recent exposure to antibiotics, comorbidities, and local trends in antibiotic resistance.

In previously healthy patients with no exposure to antibiotics within the previous 90 days, use a macrolide or doxycycline (weak recommendation).

In patients with comorbidities such as chronic disease of the heart, lung, liver, or kidneys; diabetes mellitus; alcoholism; malignancy; immunosuppression (drug- or disease-induced); or use of antimicrobials within the last 90 days, use a respiratory fluoroquinolone or beta-lactam plus a macrolide.

If the patient was exposed to antibiotics within the previous 90 days for systemic treatment of any type of bacterial infection, an alternative agent from a different class should be selected for treatment of the current illness.

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Inpatient Empiric Antibiotic Therapy

According to the 2009 Centers for Medicare and Medicaid Services (CMS) and Joint Commission consensus guidelines, inpatient treatment of pneumonia should be given within 6 hours of hospital admission (or in the emergency department if this is where the patient initially presented) and should consist of the following antibiotic regimens,[60] which are also in accordance with IDSA/ATS guidelines.[16]

For non-intensive care unit (ICU) patients, choose one option below:

  • Beta-lactam (intravenous [IV] or intramuscular [IM] administration) plus macrolide (IV or oral [PO])
  • Beta-lactam (IV or IM) plus doxycycline (IV or PO)
  • Antipneumococcal quinolone monotherapy (IV or IM)
  • If the patient is younger than 65 years with no risk factors for drug-resistant organisms, administer macrolide monotherapy (IV or PO)

For ICU patients, choose one option below:

  • IV beta-lactam plus IV macrolide
  • IV beta-lactam plus IV antipneumococcal quinolone
  • If the patient has a documented beta-lactam allergy, administer IV antipneumococcal quinolone plus IV aztreonam

For patients at increased risk of infection with Pseudomonas (acceptable for both ICU and non-ICU patients), choose one option below:

  • IV antipseudomonal beta-lactam plus IV antipseudomonal quinolone (PO quinolone in non-ICU patients only)
  • IV antipseudomonal beta-lactam plus IV aminoglycoside plus one of the following: (1) IV macrolide; (2) IV antipneumococcal quinolone (PO in non-ICU patients only); or (3) if the patient has a documented beta-lactam allergy, administer IV aztreonam plus IV aminoglycoside plus IV antipneumococcal quinolone (PO quinolone in non-ICU only)
  • The question of the need for “double coverage” for possible drug-resistant pseudomonal organisms often arises when treating critically ill patients. The use of 2 antipseudomonal medications should only be considered in critically ill patients who are at high risk for infection with drug-resistant organisms. Double coverage should be given as initial therapy early in the course of treatment, if at all, in order to make an impact in the disease course.
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Aspiration Pneumonia Empiric Therapy

Although the causative organisms in aspiration pneumonia have been noted to be similar to those of CAP or HCAP, patients with severe periodontal disease, putrid sputum, or a history of alcoholism with suspected aspiration pneumonia may be at greater risk of anaerobic infection. One of the following antibiotic regimens is suggested for such patients:[9, 16]

  • Piperacillin-tazobactam
  • Imipenem
  • Clindamycin or metronidazole plus a respiratory fluoroquinolone plus ceftriaxone

MRSA Empiric Antibiotic Therapy

For suspected infection with methicillin-resistant S aureus (MRSA), vancomycin or linezolid may be added to the antibiotic regimen until the organism's identity and antibiotic sensitivities are known, at which point the medications can be adjusted accordingly. Note, however, that when 9 studies were combined in a meta-analysis, linezolid was not superior in terms of higher cure rates for MRSA pneumonia when compared with the glycopeptides vancomycin and teicoplanin.[61] In addition, neither vancomycin nor linezolid is an optimal agent for the treatment of methicillin-sensitive S aureus (MSSA).[16]

Other agents that may be considered for use against MRSA include clindamycin, trimethoprim-sulfamethoxazole (TMP-SMZ), gentamicin, ciprofloxacin, and rifampin. More antibiotics are being evaluated for activity against MRSA.[62]

Bacterial Pneumonia and Viral Infection

The influenza pandemic of 1918 was responsible for the deaths of approximately 40-50 million people worldwide (>600,000 deaths in the United States), many of which were likely ultimately due to secondary bacterial infection.[14]

With the 2009 H1N1 influenza A pandemic, the US Centers for Disease Control and Prevention (CDC) mortality estimates range from 8,800 to 18,000 between April 2009 and April 2010. The vast majority of deaths occurred in individuals younger than 65 years.[63] Evaluation of 77 postmortem lung specimens by the CDC revealed that 29% of those that died also had evidence of bacterial coinfection.[64]

Such statistics highlight the importance of the prevention of influenza spread with vaccination and treatment with antiviral drugs, as well as place focus on the diagnosis of, treatment of, and prophylaxis against bacterial pathogens with appropriate antibiotics and pneumococcal vaccination.[14]

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Supportive Measures

Supportive measures include the following (some were mentioned previously):

  • Analgesia and antipyretics
  • Chest physiotherapy
  • Intravenous fluids (and, conversely, diuretics) if indicated
  • Monitoring – Pulse oximetry with or without cardiac monitoring, as indicated
  • Oxygen supplementation
  • Positioning of the patient to minimize aspiration risk
  • Respiratory therapy, including treatment with bronchodilators and N -acetylcysteine
  • Suctioning and bronchial hygiene – Pulmonary toilet may include active suction of secretions, chest physiotherapy, positioning to promote dependent drainage, and incentive spirometry to enhance elimination of purulent sputum and to avoid atelectasis.
  • Ventilation with low tidal volumes (6 mL/kg of ideal body weight) in patients requiring mechanical ventilation secondary to bilateral pneumonia or acute respiratory distress syndrome (ARDS)[16]
  • Systemic support may include proper hydration, nutrition, and mobilization to create a positive host milieu to fight infection and speed recovery. Early mobilization of patients, with encouragement to sit, stand, and walk when tolerated, speeds recovery.
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Clinical Resolution

Clinical response to antibiotic therapy should be evaluated within 48-72 hours of initiation. With appropriate antibiotic therapy, improvement in the clinical manifestations of pneumonia should be observed in 48-72 hours. Because of the time required for antibiotics to act, antibiotics should not be changed within the first 72 hours unless marked clinical deterioration occurs. With pneumococcal pneumonia, the cough usually resolves within 8 days and crackles heard on auscultation clear within 3 weeks.

The timing of radiologic resolution of pneumococcal pneumonia varies with patient age and the presence or absence of an underlying lung disease. The chest radiograph usually clears within 4 weeks in patients younger than 50 years without underlying pulmonary disease. In contrast, resolution may be delayed for 12 weeks or longer in older individuals and those with underlying lung disease.

Pneumonia that does not respond to treatment poses a clinical dilemma and is a common concern. If patients do not improve within 72 hours, an organism that is not susceptible or is resistant to the initial empiric antibiotic regimen should be considered. Lack of response may also be secondary to a complication such as empyema or abscess formation.

Also consider broadening the differential diagnosis to include noninfectious etiologies such as malignancies, inflammatory conditions, or congestive heart failure. In patients in whom a precipitating factor was tumoral obstruction of an airway, the infiltrate may fail to clear, or the tumor may be depicted on a chest radiograph. Computed tomography (CT) scanning may be helpful in unclear cases and in delineating more complex pulmonary processes. Carefully review the patient's medical history, especially in regard to potential exposure. See Diagnosis.

Diagnostic testing may require more complex studies when the cause of disease is less apparent. Unresponsive cases of pneumonia may require fiberoptic bronchoscopy or open lung biopsy for definitive diagnosis. Bronchoscopy helps evaluate for obstruction due to a foreign body or malignancy; transbronchial biopsy may be helpful in some cases. Lung biopsy may need to be performed if all other procedures do not aid in diagnosis and the illness continues; biopsy may be performed under CT guidance, with the aid of thoracoscopy, or with open thoracotomy. See Workup.

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Prevention

Prevention of CAP and nosocomial pneumonia are briefly discussed in this section.

Prevention of community-acquired pneumonia

Administration of influenza vaccine decreases fall and/or winter risk of viral influenza, which decreases the risk of bacterial superinfection. This vaccine is especially important in patients who are elderly and in those with comorbidity. In fact, influenza vaccination for elderly individuals results in a 48-57% reduction of the rate of hospitalization for pneumonia and influenza.

Unfortunately, although pneumococcal vaccines are effective, they are underused. Streptococcus pneumoniae is the most common cause of fatal pneumonia and pneumonia overall. The incidence of pneumococcal disease is the highest in children younger than 2 years and in adults older than 65 years. Other important risk factors are chronic heart disease, chronic lung disease, cigarette smoking, and asplenia.

A 23-valent capsular polysaccharide vaccine (Pneumovax 23) and a 13-valent protein-polysaccharide conjugate vaccine (Prevnar 13) are currently available in the United States. Both vaccines are efficacious in the prevention of invasive pneumococcal disease. The role of the pneumococcal vaccine has not been defined as clearly as that of the influenza vaccine in adults. Pneumococcal 13-valent conjugate vaccine is approved for children aged 6 weeks to 5 years and adults aged 50 years or older. The pneumococcal 23-valent vaccine is approved for adults aged 50 years or older and persons aged 2 years or older who are at increased risk for pneumococcal disease.

The CDC's Advisory Committee on Immunization Practice recommends the pneumococcal-23 vaccine for persons older than 65 years and for younger patients with chronic illnesses. In addition, administer pneumococcal vaccines to asplenic, transplant, and renal patients, as well as consider vaccinating individuals with comorbidities.

Emphasize smoking cessation to patients.

Go to Community-Acquired Pneumonia for complete information on this topic.

Prevention of nosocomial pneumonia

A number of preventative strategies have been applied in the prevention of nosocomial pneumonia. Some of these probably are effective or promising, and some are currently being evaluated.

The efficacious regimens are hand washing and isolation of patients with multiple resistant respiratory tract pathogens. Hand washing between patient contacts is a basic and often neglected behavior by medical personnel.

Interventions that should be considered or undertaken include nutritional support, attention to the size and nature of the gastrointestinal reservoir of microorganisms, careful handling of ventilator tubing and associated equipment, subglottic secretion drainage, and lateral-rotation bed therapy.

Go to Nosocomial Pneumonia for complete information on this topic.

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Complications

Potential complications of bacterial pneumonia include the following:

  • Destruction and fibrosis/organization of lung parenchyma, with scarring potential
  • Bronchiectasis
  • Necrotizing pneumonia
  • Frank cavitation
  • Empyema
  • Pulmonary abscess
  • Respiratory failure
  • Acute respiratory distress syndrome
  • Ventilator dependence
  • Superinfection
  • Death
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Consultations

Consultation with infectious disease and/or pulmonary specialists is suggested in difficult cases. In addition, a pharmacist and/or infection control specialist may be of assistance in providing information on hospital or regional bacterial resistance and sensitivity patterns.

Patients requiring noninvasive mechanical ventilation or intubation may need consultation with a critical care medicine specialist to aid in management after admission to the intensive care unit (ICU).

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Long-Term Monitoring

When a patient with bacterial pneumonia is treated in an outpatient setting, arranging adequate follow-up evaluations is mandatory. The patient should also be instructed to return if their condition deteriorates.

Patients should have a follow-up chest radiograph in approximately 6 weeks to ensure resolution of consolidation and to assess persistent abnormality of the lung parenchyma (eg, scarring, bronchiectasis). Chest radiograph findings indicating nonresolution of symptoms should raise the consideration of an endobronchial obstruction as a cause of postobstructive pneumonia. A computed tomograph (CT) scan may be of benefit in these cases.

Although guidelines have routinely recommended follow-up chest radiography in order to exclude underlying lung cancer, studies have found that the incidence of lung cancer following pneumonia is relatively low. A study by Tang et al suggests that age 50 years and above, male sex, and smoking are the only characteristics independently associated with a new lung cancer diagnosis.[65]

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Contributor Information and Disclosures
Author

Nader Kamangar, MD, FACP, FCCP, FCCM  Associate Professor of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, University of California, Los Angeles, David Geffen School of Medicine, Olive View-UCLA Medical Center; Associate Program Director, Pulmonary and Critical Care Multi-Campus Fellowship Program, Cedars-Sinai/West Los Angeles Veterans Affairs/Los Angeles Kaiser Permanente/Olive View-UCLA Medical Center; Site Director, Pulmonary/Critical Care Fellowship Program, Olive View-UCLA Medical Center

Nader Kamangar, MD, FACP, FCCP, FCCM is a member of the following medical societies: American Academy of Sleep Medicine, American Association of Bronchology, American College of Chest Physicians, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, California Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Annie Harrington, MD  Fellow in Pulmonary and Critical Care Medicine, Cedars-Sinai Medical Center

Annie Harrington, MD is a member of the following medical societies: Alpha Omega Alpha and American College of Chest Physicians

Disclosure: Nothing to disclose.

Christina Rager, MD  Resident Physician, Internal and Emergency Medicine, Olive View-University of California at Los Angeles Medical Center

Christina Rager, MD is a member of the following medical societies: American College of Physicians, American Medical Student Association/Foundation, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Dana A Stearns, MD  Assistant Director of Undergraduate Education, Department of Emergency Medicine, Massachusetts General Hospital

Dana A Stearns, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

James M Stephen, MD, FAAEM, FACEP  Assistant Professor, Tufts University School of Medicine; Attending Physician, Director of Medical Informatics and Graduate Education, Department of Emergency Medicine, Tufts Medical Center

James M Stephen, MD, FAAEM, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Ryland P Byrd Jr, MD  Professor, Department of Internal Medicine, Division of Pulmonary Medicine and Critical Care Medicine, Program Director of Pulmonary Diseases and Critical Care Medicine Fellowship, East Tennessee State University, James H Quillen College of Medicine; Medical Director of Respiratory Therapy, James H Quillen Veterans Affairs Medical Center

Ryland P Byrd Jr, MD is a member of the following medical societies: American College of Chest Physicians and American Thoracic Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Paul Blackburn, DO, FACOEP, FACEP  Attending Physician, Department of Emergency Medicine, Maricopa Medical Center

Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Medical Association, and Arizona Medical Association

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP  Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD  Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Professor and Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Sat Sharma, MD, FRCPC,to the development and writing of a source article.

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Bacterial pneumonia. Radiographic images in a patient with right upper lobe pneumonia. Note the increased anteroposterior chest diameter, which is suggestive of chronic obstructive pulmonary disease (COPD).
Bacterial pneumonia. Radiographic images in a patient with bilateral lower lobe pneumonia. Note the spine sign, or loss of progression of radiolucency of the vertebral bodies
Bacterial pneumonia. Radiographic images in a patient with early right middle lobe pneumonia.
Table. Pathogen-Driven Antibiotic Choices[16]
OrganismFirst-Line AntimicrobialsAlternative Antimicrobials
Streptococcus pneumoniae
Penicillin susceptible



(MIC < 2 mcg/mL)



Penicillin G, amoxicillinMacrolide, cephalosporin (oral or parenteral), clindamycin, doxycycline, respiratory fluoroquinolone
Penicillin resistant



(MIC ≥2 mcg/mL)



Agents chosen on the basis of sensitivityVancomycin, linezolid, high-dose amoxicillin (3 g/d with MIC ≤4 mcg/mL
Staphylococcus aureus
Methicillin susceptibleAntistaphylococcal penicillinCefazolin, clindamycin
Methicillin resistantVancomycin, linezolidTrimethoprim- sulfamethoxazole
Haemophilus influenzae
Non–beta-lactamase producingAmoxicillinFluoroquinolone, doxycycline, azithromycin, clarithromycin
Beta-lactamase producingSecond- or third-generation cephalosporin, amoxicillin/clavulanateFluoroquinolone, doxycycline, azithromycin, clarithromycin
Mycoplasma pneumoniaeMacrolide, tetracyclineFluoroquinolone
Chlamydophila pneumoniaeMacrolide, tetracyclineFluoroquinolone
Legionella speciesFluoroquinolone, azithromycinDoxycycline
Chlamydophila psittaciTetracyclineMacrolide
Coxiella burnetiiTetracyclineMacrolide
Francisella tularensisDoxycyclineGentamicin, streptomycin
Yersinia pestisStreptomycin, gentamicinDoxycycline, fluoroquinolone
Bacillus anthracis (inhalational)Ciprofloxacin, levofloxacin, doxycyclineOther fluoroquinolones, beta-lactam (if susceptible), rifampin, clindamycin, chloramphenicol
EnterobacteriaceaeThird-generation cephalosporin, carbapenemBeta-lactam/beta-lactamase inhibitor, fluoroquinolone
Pseudomonas aeruginosaAntipseudomonal beta-lactam plus ciprofloxacin, levofloxacin, or aminoglycosideAminoglycoside plus ciprofloxacin or levofloxacin
Bordetella pertussisMacrolideTrimethoprim- sulfamethoxazole
Anaerobe (aspiration)Beta-lactam/beta-lactamase inhibitor, clindamycinCarbapenem
MIC = Minimal inhibitory concentration.
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