eMedicine Specialties > Infectious Diseases > Lower Respiratory Tract Infections

Pneumonia, Community-Acquired: Treatment & Medication

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
Contributor Information and Disclosures

Updated: Jul 24, 2009

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.
Empiric therapy in hospitalized patients with community-acquired pneumonia
Suboptimal regimens include the following:
  • 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)
Optimal regimens include the following:
  • Monotherapy
    • Typical CAP pathogens
      • Respiratory quinolone
      • Ceftriaxone
      • Ertapenem
    • Typical CAP pathogens
      • Respiratory quinolone
      • Doxycycline
Empiric therapy for CAP in patients with HIV infection is as follows:
  • 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.

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

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 - 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.

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

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

Documented hypersensitivity; avoid in pregnancy and children <8 y

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.

Adult

500 mg PO qd for 7-14 d

Pediatric

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

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

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.

Adult

400 mg PO/IV qd

Pediatric

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

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

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

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.

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

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

Documented hypersensitivity to drug or amide-type anesthetics

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.

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

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

Documented hypersensitivity; hepatic impairment; do not administer with pimozide

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.

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

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

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

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References
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Further Reading

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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

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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
Disclosure: Nothing to disclose.

 
 
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