Community-acquired pneumonia

S pneumoniae
M pneumoniae
C pneumoniae
H influenzae
Respiratory viruses1
Legionella species
Gram-negative bacilli
Anaerobes (aspiration)
S aureus

1Influenza A and B, adenovirus, respiratory syncytial virus, and parainfluenza.

Data from Mandell LA et al. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis. 2007;44:227–72.


Streptococcus pneumoniae

Klebsiella pneumoniae

Haemophilus influenzae, and gram-negative rods are the causative organisms.

viral infections (adenoviruses, respiratory syncytial virus [RSV]) and bacterial infections not seen in lobar pneumonias:


Legionella, and Chlamydia .

Staphylococcus aureus, Streptococcus pyogenes, or H. influenzae .

Pseudomonas aeruginosa (especially in patients on ventilators), Klebsiella, and Escherichia coli . P. aeruginosa is also a common cause of pneumonia and chronic infection in patients with cystic fibrosis (CF).

Pneumocystis pneumonia (PCP) is caused by Pneumocystis jiroveci and is the most common pneumonia causing pathogen in patients with AIDS (CD4 count < 200/μ).

S. pneumoniae
M. pneumoniae
C. pneumoniae
H. influenzae
Legionella spp.
Respiratory viruses
  • In a study of children hospitalized with CAP (N = 254), the cause of the disease (identified in 85% of cases) was most often viral (62%, with 30% having evidence of both viral and bacterial pathogens).9 The most common pathogens were Streptococcus pneumoniae (37%), respiratory syncytial virus (29%), and rhinovirus (24%). Dual bacterial infections were found in 19 patients; only 1 patient of 125 tested had a positive blood culture.
  • In a single U.S. hospital study, pathogens identified in adult patients with CAP separate from HCAP (N = 208) were S. pneumoniae (40.9%), Haemophilus influenzae (17.3%), Staphylococcus aureus (13.5%) and methicillin-resistant S. aureus (MRSA, 12%).10 For HCAP, the most common pathogens were MRSA (30.6%) and Pseudomonas aeruginosa (25.5%). This distribution of pathogens for HCAP may be unique to this setting.
  • Mycobacterium tuberculosis (TB), fungi, Legionella, and many respiratory viruses are spread by aerosolization. Reported incidence rates of atypical pathogens vary greatly; for example, Legionella species were identified in patients with CAP in 1.3% (defined as positive urine antigen),10 1.4% (defined as 4-fold rise in antibody titer or a single titer of ≥400),11 and 18.9% (defined as 4-fold rise in antibody titer of 128),12 with coinfection with another pathogen in approximately 10%.
  • Etiology is unknown in up to 70% of cases of CAP.
S. pneumoniae
M. pneumoniae
C. pneumoniae
H. influenzae
Legionella spp.
Respiratory viruses


Most common route of infection is microaspiration of oropharyngeal secretions colonized by pathogens. In this setting, S. pneumoniae and H. influenzae are the most common pathogens.

Pneumonia secondary to gross aspiration occurs postoperatively or in those with central nervous system disorders; anaerobes and Gram-negative bacilli are common pathogens.

Hematogenous spread

Hematogenous spread, most often from the urinary tract, results in Escherichia coli pneumonia, and hematogenous spread from intravenous catheters or in the setting of endocarditis may cause S. aureus pneumonia.






Pneumonia is an infection in the lower respiratory tract (distal airways, alveoli, and interstitium of the lung).


Pneumonia is usually caused by infection with viruses or bacteria and less commonly by other microorganisms, certain medications and conditions such asautoimmune diseases.[2][5] Risk factors include other lung diseases such as cystic fibrosisCOPD, and asthmadiabetesheart failure, a history of smoking, a poor ability to cough such as following a stroke, or a weak immune system.[6] Diagnosis is often based on the symptoms and physical examinationChest X-ray, blood tests, and culture of the sputum may help confirm the diagnosis.[7] The disease may be classified by where it was acquired with community, hospital, or health care associated pneumonia.[8]

Vaccines to prevent certain types of pneumonia are available. Other methods of prevention include handwashing and not smoking.[9] Treatment depends on the underlying cause.[10] Pneumonia believed to be due to bacteria is treated withantibiotics.[11] If the pneumonia is severe, the affected person is generally hospitalized.[10] Oxygen therapy may be used if oxygen levels are low.[11]

Pneumonia affects approximately 450 million people globally (7% of the population) and results in about 4 million deaths per year.[12][13] Pneumonia was regarded byWilliam Osler in the 19th century as "the captain of the men of death".[14] With the introduction of antibiotics and vaccines in the 20th century survival improved.[12]Nevertheless, in developing countries, and among the very old, the very young, and the chronically ill, pneumonia remains a leading cause of death.[12][15] Pneumonia often shortens suffering among those already close to death and has thus been called "the old man's friend".[16]


United States

Pneumonia is the seventh leading cause of death in the United States.

Pneumonia affects approximately 450 million people globally (7% of the population) and results in about 4 million deaths per year.[12][13] Pneumonia was regarded byWilliam Osler in the 19th century as "the captain of the men of death".[14] With the introduction of antibiotics and vaccines in the 20th century survival improved.[12]Nevertheless, in developing countries, and among the very old, the very young, and the chronically ill, pneumonia remains a leading cause of death.[12][15] Pneumonia often shortens suffering among those already close to death and has thus been called "the old man's friend".[16]





The World Health Organization estimates that lower respiratory tract infection is the most common infectious cause of death in the world (the third most common cause overall), with almost 3.5 million deaths yearly.1




  • The majority of hospitalized patients with community-acquired pneumonia can be treated with either a respiratory fluoroquinolone or a combination of cephalosporin and a macrolide.

  • Alternative antibiotic treatment should be based on the presence of multiple risk factors for health care–associated pneumonia, specific risks (e.g., structural lung disease), or uniquely characteristic syndromes (e.g., the toxin-mediated, community-acquired, methicillin-resistant Staphylococcus aureus syndrome).

  • The current criteria for health care–associated pneumonia result in excessive use of broad-spectrum antibiotic agents. The presence of multiple pneumonia-specific alternative risk factors may allow focused diagnostic testing and treatment.

  • Patients with three or more minor criteria for severe community-acquired pneumonia (e.g., elevated blood urea nitrogen, confusion, and a high respiratory rate) should receive extensive intervention in the emergency department and be considered for admission to the intensive care unit.

Community-acquired pneumonia that is severe enough to require hospitalization is associated with excess mortality over the subsequent years among survivors,4-6 even among young people without underlying disease.5 Admission to the hospital for community-acquired pneumonia is also costly, especially if care in an intensive care unit (ICU) is required.7


The most common microbiologic agent of pneumonia is often not isolated (Table 16-1). Furthermore, studies have shown that bacteriologic causes of pneumonia cannot be determined by radiographic appearance (i.e., “typical” vs. “atypical”). In the proper clinical setting, certain clinical microbes should be considered because they can affect treatment considerations and epidemiologic studies. These include Legionella spp., influenza A and B, and community-acquired methicillin-resistant Staphylococcus aureus (MRSA).

Community Acquired

   Streptococcus pneumoniae
   Mycoplasma pneumoniae
   Haemophilus influenzae
   Chlamydophila pneumoniae
   Respiratory viruses[∗]



Fever, pleuritic chest pain, and dyspnea are common symptoms. In elderly patients, CAP may present with mental status changes. Although its absence usually makes pneumonia less likely, fever can be absent in the elderly patient.


Cough, sputum production. Physical examination findings include an elevated respiratory rate, conversational dyspnea, tachycardia, and rales. Egophony and dullness to percussion may be noted with focal consolidation.

Laboratry Tests

Typical laboratory findings include leukocytosis. The diagnosis of pneumonia is based on the presence of symptoms and

Radiological Exams

Presence of an infiltrate on chest radiograph. If infiltrate is not present, consider obtaining a chest tomography scan (which has higher sensitivity).




A 67-year-old woman with mild Alzheimer's disease who has a 2-day history of productive cough, fever, and increased confusion is transferred from a nursing home to the emergency department. She has had no recent hospitalizations or recent use of antibiotic agents. Her temperature is 38.4°C (101°F), the blood pressure is 145/85 mm Hg, the respiratory rate is 30 breaths per minute, the heart rate is 120 beats per minute, and the oxygen saturation is 91% while she is breathing ambient air. Crackles are heard in both lower lung fields. She is oriented to person only. The white-cell count is 4000 per cubic millimeter, the serum sodium level is 130 mmol per liter, and the blood urea nitrogen is 25 mg per deciliter (9.0 mmol per liter). A radiograph of the chest shows infiltrates in both lower lobes.

How and where should this patient be treated?


1. Modified from Mandell LA, Wunderink RG, Anzueto A, et al. Infectious Diseases Society–American Thoracic Society Consensus Guidelines on Management of Community-Acquired Pneumonia in Adults. Clin Infect Dis 2007;44:S27-S72.








Table 16-1   -- Most Common Etiologies of Community-Acquired Pneumonia
Patient Type Etiology

Certain diagnostic tests are performed based on clinical setting. Blood cultures are not routinely done in the outpatient setting but should always be done if the patient is being admitted to the hospital, ideally before antibiotics are given. The use of Gram stain and sputum culture remains controversial but can provide more evidence of a bacterial cause (e.g., many PMNs). If sputum cultures are being obtained, it is recommended that the physician have the patient expectorate directly into a specimen cup and have it sent immediately for processing. This can increase the yield of isolating Streptococcus pneumoniae among other respiratory pathogens. Other tests include urine antigen tests for S. pneumoniae, Legionella pneumophila serogroup 1, and nasal swab for influenza A and B. In young children, RSV, adenovirus, and parainfluenza in addition to influenza are common causes. Nasal swab for RSV and influenza can be rapidly done, but the other causes can be determined with viral cultures, serology, enzyme-linked immunosorbent assay (ELISA), and polymerase chain reaction (PCR), although results usually are received after resolution of the acute symptoms.

Perhaps the most important decision for clinicians is to determine the location of treatment. The American Thoracic Society (ATS) and the Infectious Diseases Society of America (IDSA) recommend use of the pneumonia severity index (PSI), which uses 20 variables to risk-stratify the patient into five mortality classes, or the CURB-65, which measures five clinical variables in this decision making. The CURB-65 may be the easiest and most convenient to use at the site of decision making. A score of 0 or 1 indicates treatment as an outpatient; a score of 2 requires hospital admission to the general medical ward; and a score of 3 or more indicates admission to an intensive care unit (ICU) (Box 16-1). Box 16-1 

CURB-65 Criteria

Assign a value of 1 for each variable:

       Confusion: Is the patient disoriented to person, place, or time?
       BUN >20 mg/dl
       Respiratory rate > 30 breaths/min
       Blood pressure: systolic <90 or diastolic <60 mm Hg
       Age >65 years


       Score 0 or 1: outpatient treatment
       Score 2 : inpatient treatment on a general medical floor
       Score >3: inpatient treatment in an intensive care unit

BUN, Blood urea nitrogen.

Treatment of CAP should be targeted toward the most likely etiology (Table 16-2). Outpatient therapy for patients who have no comorbidities and have not received antibiotics within the last 3 months includes doxycycline or a macrolide antibiotic. Use of a fluoroquinolone antibiotic (levofloxacin or moxifloxacin) should be reserved for patients with more complicated pneumonia and those requiring hospitalization. Patients who have comorbid conditions or recent antibiotic exposure, or who will be hospitalized, should receive a respiratory fluoroquinolone or combination therapy with a beta-lactam drug plus a macrolide, for 48 to 72 hours after fever abates (usually 5-7 days’ total therapy). If an organism is isolated, therapy may be narrowed to cover the causative agent. The clinician should consider longer therapy and appropriate antibiotics to cover for infection by less common organisms such as Staphylococcus aureus or Pseudomonas aeruginosa. If the patient has no more than one abnormal value (temperature <37.8° C, heart rate <100, respiratory rate <24, SBP >90, O2 saturation >90%, Po2 >60 on room air) and the patient is able to maintain oral intake and has a normal mental status, the clinician can safely switch to oral therapy and discharge the patient from the hospital. Unless the etiology of the pneumonia is known, the physician should switch to oral antibiotics in the same class as the intravenous antibiotics used.

Table 16-2   -- Guide to Empiric Choice of Antimicrobial Agent for Treating Patients with Community-Acquired Pneumonia (CAP)
Patient Characteristics Preferred Treatment Options
Previously Healthy
No recent antibiotic therapy Oral-based β-lactam, macrolide,[∗] or doxycycline
Recent antibiotic therapy[†] A respiratory fluoroquinolone[‡] alone, an advanced macrolide[∗] plus high-dose amoxicillin,[§] or an advanced macrolide plus high-dose amoxicillin-clavulanate.[¶]
Comorbidities (COPD, diabetes, renal failure or congestive heart failure, or malignancy)
No recent antibiotic therapy An advanced macrolide[∗] plus β-lactam or a respiratory fluoroquinolone
Recent antibiotic therapy A respiratory fluoroquinolone[‡] alone or an advanced macrolide plus a β-lactam[∗∗]
Suspected aspiration with infection Amoxicillin-clavulanate or clindamycin
Influenza with bacterial superinfection Vancomycin, linezolid, or other coverage for MRSA or community-acquired MRSA
Medical Ward
No recent antibiotic therapy A respiratory fluoroquinolone alone or an advanced macrolide plus a β-lactam[††]
Recent antibiotic therapy An advanced macrolide plus a β-lactam, or a respiratory fluoroquinolone alone (regimen selected will depend on nature of recent antibiotic therapy)
Intensive Care Unit (ICU)
Pseudomonas infection is not an issue A β-lactam[††] plus either an advanced macrolide or a respiratory fluoroquinolone
Pseudomonas infection is not an issue but patient has a β-lactam allergy A respiratory fluoroquinolone, with or without clindamycin
Pseudomonas infection is an issue[‡‡] (cystic fibrosis, impaired host defenses) Either (1) an antipseudomonal β-lactam[§§] plus ciprofloxacin, or (2) an antipseudomonal agent plus an aminoglycoside[##] plus a respiratory fluoroquinolone or a macrolide
   Pseudomonas infection is an issue but the patient has a β-lactam allergy.
   Health care–associated exposure
   Aztreonam plus aminoglycoside plus levofloxacin[¶¶] or other respiratory quinolone
   Anti-Pseudomonas cephalosporin, carbapenem (not ertapenem) or β-lactam/β-lactamase inhibitor with anti-Pseudomonas activity plus vancomycin (for MRSA coverage) ± quinolone or aminoglycoside
Nursing Home
Receiving treatment in nursing home A respiratory fluoroquinolone alone or vancomycin (for S. aureus including MRSA) plus a β-lactam (cefepime or piperacillin/tazobactam if Pseudomonas is suspected; ceftriaxone if Pseudomonas is not suspected)
Hospitalized Same as for medical ward and ICU
Data from Mandell LA, Wunderink RG, Anzueto A, et al. Infectious Diseases Society of America/American Thoracic Society consensus guidelines of community-acquired pneumonia in adults. Clin Infect Dis. 2007;44:S27-S72.

COPD, Chronic obstructive pulmonary disease; MRSA, methicillin-resistant Staphylococcus aureus.

Azithromycin or clarithromycin.
That is, the patient was given a course of antibiotic(s) for treatment of any infection within the past 3 months, excluding the current episode of infection. Such treatment is a risk factor for drug-resistant Streptococcus pneumoniae and possibly for infection with gram-negative bacilli. Depending on the class of antibiotics recently given, one or another of the suggested options may be selected. Recent use of a fluoroquinolone should dictate selection of a nonfluoroquinolone regimen, and vice versa.
Moxifloxacin, levofloxacin, or gemifloxacin.
§ Dosage: 1 g orally (PO) three times daily (tid).
Dosage: 2 g PO twice daily (bid).
∗∗ High-dose amoxicillin (1 g tid), high-dose amoxicillin-clavulanate (2 g bid), cefpodoxime, cefprozil, or cefuroxime.
†† Cefotaxime, ceftriaxone, ampicillin-sulbactam, or ertapenem.
‡‡ The antipseudomonal agents chosen reflect this concern. Risk factors for Pseudomonas infection include severe structural lung disease (e.g., bronchiectasis) and recent antibiotic therapy, health care–associated exposures or stay in hospital (especially in the ICU). For patients with CAP in the ICU, coverage for S. pneumoniae and Legionella species must always be considered. Piperacillin-tazobactam, imipenem, meropenem, and cefepime are excellent β-lactams and are adequate for most S. pneumoniae and H. influenzae infections. They may be preferred when there is concern for relatively unusual CAP pathogens, such as P. aeruginosa, Klebsiella spp., and other gram-negative bacteria.
§§ Piperacillin, piperacillin-tazobactam, imipenem, meropenem, or cefepime.
## Data suggest that older adults receiving aminoglycosides have worse outcomes.
¶¶ Dosage for hospitalized patients, 750 mg/day.

The U.S. Preventive Services Task Force (USPSTF) along with IDSA and ATS recommend annual influenza vaccinations to those over 50 years of age, those who are (or who reside with those who are) at high risk for influenza complications, and all health care workers. Furthermore, the pneumococcal vaccine should be given to all those over age 65. Smoking cessation is also important and should be discussed at each clinic visit.


   Locally adapted guidelines should be implemented to improve the processing of care variables and relevant clinical outcomes in pneumonia (Mandell et al., 2007) (SOR: B).
   Objective criteria or scores should always be supplemented with physician determination of subjective factors, including the patient’s ability to take oral medication safely and reliably and the availability of outpatient support resources (Mandell et al., 2007) (SOR: B).
   For patients with CURB-65 score of 2 or higher, more intensive treatment (i.e., hospitalization or, where appropriate and available, intensive in-home health care services) is usually warranted (Mandell et al., 2007) (SOR: C).


Anthony Zeimet
Key Points

       Concerns about development of resistant seasonal and H1N1 swine-derived influenza virus should be considered in the decision to administer antiviral medications to healthy patients with these infections.
       The abrupt onset of fever with chills, headache, malaise, myalgias, arthralgias, and rigors during “flu season” is sufficient to diagnose influenza.
       Prevention of influenza is generally with vaccination.

Influenza deserves special mention because it is an important cause of pneumonitis and can precede a bacterial pneumonia. Influenza viruses are medium-sized enveloped ribonucleic acid (RNA) viruses that consist of a lipid bilayer with matrix proteins with spiked surface projections of glycoproteins (hemagglutinins, neuraminidase) on the outer surface (Figure 16-1). Both influenza A and influenza B have eight segmented pieces of single-stranded RNA. The only difference between influenza A and B is that B does not have an M2 ion channel. Hemagglutinins, three types of which typically infect humans (H1, H2, H3), bind to respiratory epithelial cells and allow fusion with the host cell. Neuraminidase, consisting of two types (N1, N2), allows release of virus from the infected cells.

Click to view full size figure

Figure 16-1  Schematic model of influenza A virus.
(From Treanor JJ: Influenza viruses, including avian influenza and swine influenza. In Mandell GL, Bennett JE, Dolin RD (eds). Mandell, Douglas, and Bennett’s Principles and Practices of Infectious Diseases, 7th ed. Philadelphia, Churchill Livingstone, 2010, p 2266.)

A unique aspect of influenza is that antigenic variation occurs annually. Antigenic shift is caused by a genetic reassortment between animal and human influenza strains, producing a novel virus that generally causes the worldwide pandemics. Influenza viruses circulate mostly among humans, birds, and swine. Sometimes; a human strain and an animal strain can intermingle and create a new, unique virus. This is what happened during spring 2009, heralding the most recent pandemic and creating “Novel H1N1 Influenza” (swine influenza). Genotype analysis of this strain determined that components came from an influenza virus circulating among swine herds in North America that combined with a virus circulating among ill swine in Eurasia, creating a new influenza strain capable of causing disease in humans. Because this virus had not previously infected humans, it had the potential to cause widespread morbidity and mortality worldwide. During pandemics, the U.S. Centers for Disease Control and Prevention (CDC) estimates an additional 10,000 to 40,000 deaths caused by influenza. Although higher than in nonpandemic years, mortality was significantly less than initially predicted in 2009.

The abrupt onset of fever, along with chills, headache, malaise, myalgias, arthralgias, and rigors during “flu season,” is sufficient to diagnose influenza. As the fever resolves, a dry cough and nasal discharge predominate. A rapid nasal swab or viral cultures can be used to confirm the diagnosis of influenza but is rarely needed. In fact, the sensitivity of these rapid tests can range from 50% to 70%, so a negative test does not rule out influenza. The primary care physician needs to determine if the patient has influenza or the common cold, because symptoms of both illnesses generally overlap (Table 16-3).

Table 16-3   -- Common Cold versus Influenza Symptoms
Symptom Common Cold Influenza
Fever Rare Abrupt onset
Cough Frequent, usually hacking Frequent, usually severe
Sore throat Frequent Rare
Nasal congestion Frequent Rare
Sneezing Frequent Rare
Myalgia Rare Frequent
Headache Rare Frequent
Fatigue Mild Severe

Treatment of influenza is generally not necessary because it is usually a self-limiting condition. Treatment should be reserved for those with comorbidities who present within 48 hours of symptom onset. Neuraminidase inhibitors (zanamivir and oseltamivir) prevent the release of virus from the respiratory epithelium and are approved for both influenza A and influenza B. The M2 inhibitors (amantadine and rimantadine) are approved by the U.S. Food and Drug Administration (FDA) for the treatment of influenza A because these drugs block the M2 ion protein channel, preventing fusion of the virus to host cell membrane (influenza B has no M2 ion channel). The use of M2 inhibitors is limited because of increasing resistance among influenza A viruses, as well as causing central nervous system (CNS) problems that are usually exacerbated in elderly persons, who are more likely to seek treatment for influenza (Table 16-4).

Table 16-4   -- Treatment and Chemoprophylaxis Recommendations for Influenza
Agent/Group Treatment Chemoprophylaxis
Neuraminidase Inhibitors
Adults 75-mg capsule twice daily (bid) for 5 days 75-mg capsule once daily (qd)
Children (age >12 mo)
<15 kg 60 mg/day divided into 2 doses 30 mg qd
15-23 kg 90 mg/day in 2 doses 45 mg qd
24-40 kg 120 mg/day in 2 doses 60 mg qd
>40 kg 160 mg/day in 2 doses 75 mg qd
Adults Two 5-mg inhalations (10 mg bid) Two 5-mg inhalations (10 mg qd)
Children Two 5-mg inhalations (10 mg bid)(age >7 yr) Twp 5-mg inhalations (10 mg qd)(age >5 yr)
M2 Inhibitors (Adamantadines)[∗]
Adults 200 mg/day as either a single daily dose or divided into 2 doses 200 mg/day as either a single daily dose or divided into 2 doses
1-9 yr 6.6 mg/kg/day (max, 150 mg/day) divided in 2 doses 5 mg/kg qd, not to exceed 150 mg
>10 yr 200 mg/day as either a single daily dose or divided into 2 doses 200 mg/day as either a single daily dose or divided into 2 doses
Adults 200 mg/day as either a single daily dose or divided into 2 doses 200 mg/day as either a single daily dose or divided into 2 doses
1-9 yr 5-8 mg/kg/day divided into 2 doses or as a single daily dose (max, 150 mg/day) 5-8 mg/kg/day divided into 2 doses or as a single daily dose (max, 150 mg/day)
9-12 yr 200 mg/day divided into 2 doses 200 mg/day divided into 2 doses
Modified from Harper SA, Bradley JS, Englund JA, et al. Seasonal influenza in adults and children: diagnosis, treatment, chemoprophylaxis, and institutional outbreak management. Clinical Practice Guidelines of the Infectious Diseases Society of America. Clin Infect Dis 2009;48:1003-1032.
The amantadines should be used only when influenza A (H1N1) infection or exposure is suspected. The amantadines should not be used for infection or exposure to influenza A (H2N3) or influenza B.
Rimantadine has not been approved by the U.S. Food and Drug Administration for treatment of children, although published data exist on safety and efficacy in the pediatric population.

The major complication of influenza is a secondary bacterial pneumonia or exacerbation of underlying COPD. Initial improvement in clinical symptoms followed by deterioration usually suggests a secondary bacterial pneumonia, which can usually be confirmed with a chest radiograph showing an infiltrate. Other, less common complications of influenza include myositis, myocarditis, pericarditis, transverse myelitis, encephalitis, and Guillain-Barré syndrome.

Prevention of influenza is generally with vaccination. Box 16-2 outlines patients at risk for influenza complications who should be vaccinated yearly. Although anyone wanting an influenza vaccine should be vaccinated, during periods of vaccine shortage, high-risk groups have priority. A well-matched vaccine can prevent influenza among 70% to 90% of adults and decrease work absenteeism. Conversely, a poorly matched vaccine only prevents influenza in 50% of healthy adults. Proper hand hygiene and covering one’s cough are two additional important components in preventing the spread of influenza virus.


   Early treatment (within 48 hours of onset of symptoms) with oseltamivir or zanamivir is recommended for influenza A (Jefferson et al., 2006) (SOR: A).
   Use of oseltamivir and zanamivir is not recommended for patients with uncomplicated influenza with symptoms for more than 48 hours (Kaiser and Hayden, 1999) (SOR: A).
   Oseltamivir and zanamivir may be used to reduce viral shedding in hospitalized patients or to treat influenza pneumonia (Mandell et al., 2007) (SOR: C).

Box 16-2 
Groups at risk for Influenza Complications[∗]

   Unvaccinated infants age 12 to 24 months
   Persons with asthma or other chronic pulmonary disease, such as cystic fibrosis in children or chronic obstructive pulmonary disease in adults
   Patients with hemodynamically significant cardiac disease
   Patients with immunosuppressive disorders or receiving immunosuppressive therapy
   Patient with human immunodeficiency virus (HIV) infection
   Patients with sickle cell anemia and other hemoglobinopathies
   Patients with disease requiring long-term aspirin therapy (e.g., rheumatoid arthritis, Kawasaki disease)
   Patients with chronic renal obstruction
   Patients with cancer
   Patients with chronic metabolic disease, such as diabetes mellitus
   Patient with neuromuscular disorders, seizure disorders, or cognitive dysfunction that may compromise the handling of respiratory secretions
   Adults older than 66 years
   Residents of any age of nursing homes or other long-term care facilities

Modified from Harper SA, Bradley JS, Englund JA, et al. Seasonal influenza in adults and children: diagnosis, treatment, chemoprophylaxis, and institutional outbreak management. Clinical Practice Guidelines of the Infectious Diseases Society of America. Clin Infect Dis 2009;48:1003-1032.
∗ Data suggest that the highest risk of both mortality and serious morbidity (e.g., hospitalization) occurs in severely immunocompromised patients (e.g., hematopoietic stem cell transplant patients) and very elderly (>85 years) residents of nursing homes; infants under age 24 months also have high hospitalization rates but lower case-fatality rates than the other two groups.

  • Three to 4 million adults per year in United States are diagnosed with CAP (8 to 15 per 1000 persons/year).3,4
  • Annual incidence rate of CAP requiring hospitalization: 267 per 100,000 population and 1012 per 100,000 individuals older than 65 years of age.5
  • Ten percent to 20% of patients are admitted to the hospital.3,4,6 Of those, 10% to 20% are admitted to the intensive care unit (ICU).7
  • Increased incidence in men and in blacks versus whites.3
  • CAP is the most frequent cause of death caused by infectious disease in the United States and the eighth leading cause of death overall (2007).7,8
  • Economic burden associated with CAP is estimated at more than $12 billion annually in the United States.7


Vaccines to prevent certain types of pneumonia are available. Other methods of prevention include handwashing and not smoking.

Illustrative Question

A 67-year-old man is transferred to a rehabilitation facility after being hospitalized for a hip fracture. During his hospitalization, he was diagnosed with multiple myeloma and started chemotherapy. He has no other significant medical issues and recently had a negative tuberculin skin test.

His vaccination history includes receipt of the influenza vaccine shortly before he started chemotherapy and receipt of the 23-valent pneumococcal polysaccharide vaccine 2 years ago.

Which one of the following vaccinations is recommended for this patient at this time?

» 13-valent pneumococcal conjugate vaccine
» Measles–mumps–rubella booster
» Meningococcal polysaccharide vaccine
» Herpes zoster vaccine
» 23-valent pneumococcal polysaccharide booster

13-valent pneumococcal conjugate vaccineMeasles–mumps–rubella boosterMeningococcal polysaccharide vaccine Herpes zoster vaccine23-valent pneumococcal polysaccharide booster

Key Learning Point View Case Presentation

For adults who are immunocompromised or age 65 or older, the appropriate pneumococcal vaccine strategy consists of both the 13-valent pneumococcal conjugate vaccine and the 23-valent pneumococcal polysaccharide vaccine.

Detailed Feedback

The Advisory Committee on Immunization Practices recommends both the 13-valent pneumococcal conjugate vaccine (PCV13) and the 23-valent pneumococcal polysaccharide vaccine (PPSV23) for all adults aged 65 years or older and for high-risk groups, including adults with immunocompromising conditions (including HIV infection and malignancies) and those with functional or anatomic asplenia, cerebrospinal fluid leaks, or cochlear implants. PPSV23 covers more strains, but PCV13 is more immunogenic; thus, both are recommended. Patients with multiple myeloma are at particularly high risk for invasive disease due to encapsulated organisms, especially Streptococcus pneumoniae.

Patients from high-risk groups who have not received any pneumococcal vaccines should receive PCV13 initially, followed by PPSV23 at least 8 weeks later. A one-time dose of the PPSV23 booster is recommended 5 years after the first dose for adults aged 19 to 64 years who have chronic renal failure or nephrotic syndrome, an immunocompromising condition, or functional or anatomic asplenia. Patients who received PPSV23 before age 65 should receive one more dose at age 65 or later, provided it is at least 5 years since the prior dose.

High-risk adults who have previously received at least one dose of PPSV23 should receive PCV13 no earlier than one year after the last PPSV23 dose. For those who require additional doses of PPSV23, the first such dose should be given no sooner than 8 weeks after PCV13 and no sooner than 5 years after the most recent dose of PPSV23.

This patient, who is at increased risk for infection because of malignancy, received PPSV23 two years ago and should now receive PCV13.

The meningococcal vaccine is not appropriate for this patient because it is indicated only for people with asplenia and complement deficiencies, for high-risk groups including military recruits and college students, and for people in regions with epidemic meningococcal disease.

Both the measles–mumps–rubella booster and the herpes zoster vaccines are live attenuated vaccines that are contraindicated in many immunocompromised individuals. Also, because this patient was born before 1957, he is considered immune to measles and mumps.


Centers for Disease Control and Prevention (CDC). Use of 13-valent pneumococcal conjugate vaccine and 23-valent pneumococcal polysaccharide vaccine for adults with immunocompromising conditions: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep 2012 10 12; 61:816.   > View Abstract

Tomczyk S et al. Use of 13-valent pneumococcal conjugate vaccine and 23-valent pneumococcal polysaccharide vaccine among adults aged ≥65 years: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep 2014 09 19; 63:822.   > View Abstract

Centers for Disease Control and Prevention. PCV13 (pneumococcal conjugate) vaccine: Recommendations, scenarios and Q&As for healthcare professionals about PCV13 for adults. Sep 3, 2015.

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1. Determine whether the pneumonia is community acquired, hospital acquired or health facility acquired.

Testing for a microbial diagnosis is usually not performed in outpatients because empiric treatment is almost always successful.

Empiric antibiotics (a macrolide or fluoroquinolone) were almost effective in >95 percent; only 1 percent required hospitalization due to failure of the outpatient regimen.



In the United States

Azithromycin (macrolide) – 500 mg on day 1 followed by four days of 250 mg a day or 500 mg daily for three days

Clarithromycin (macrolide) – 500 mg twice daily for five days

Clarithromycin ((macrolide) XL – Two 500 mg tablets (1000 mg per dose) once daily for five days


Doxycycline – 100 mg twice daily

United Kingdom

United Kingdom — In the 2009 British Thoracic Society guidelines, the preferred drug for outpatient management is amoxicillin (500 mg orally three times daily), with doxycycline or clarithromycin as alternatives (eg, for those with penicillin allergy) (table 3) [20].

The 2014 NICE guidelines make similar recommendations [22].

The rationale is that amoxicillin at these doses is effective against most strains of S. pneumoniae with decreased susceptibility to penicillin. Most of the macrolide-resistant S. pneumoniae in Europe is erm-mediated high-level resistance. As a result, the macrolides are not optimal first-line empiric agents. (See "Antibiotic studies for the treatment of community-acquired pneumonia in adults", section on 'Macrolide resistance' and "Resistance of Streptococcus pneumoniae to the macrolides, azalides, lincosamines, and ketolides".)

Coverage of atypical pathogens — The United Kingdom approach places less significance than the North American approach on the need to treat the atypical pathogens empirically in ambulatory patients [5,20,22]. Initial empiric therapy that covers M. pneumoniae is considered unnecessary, since the pathogen exhibits epidemic periodicity every four to five years and largely affects younger persons.

Although the clinical course of M. pneumoniae or C. pneumoniae infection is often self-limited, these pathogens can cause severe CAP. As a result, it has been argued that appropriate treatment for even mild CAP due to Mycoplasma reduces both morbidity and the duration of symptoms [26]. (See "Mycoplasma pneumoniae infection in adults".)

The efficacy of empiric coverage of atypical pathogens was evaluated in a 2005 meta-analysis that evaluated 18 randomized trials of over 6700 patients with mild to moderate CAP who were assigned to treatment with either a beta-lactam or an antibiotic active against atypical pathogens [27]. There was no overall advantage to covering atypical pathogens in terms of the rate of failure to achieve clinical cure or improvement (relative risk [RR] 0.97, 95% CI 0.87-1.07) but, in a subgroup analysis, there was a significantly lower failure rate for Legionella infection with such a regimen (RR 0.40, 95% CI 0.19-0.85). These trials were not designed to compare the time to response with the different regimens.





Therefore use doxycycline for United States patients or [ a regimen for patients with comorbidities or recent antibiotic use (described in the next section) should be given.]


For such patients, either doxycycline (if the local prevalence of doxycycline resistance is <25 percent) or a regimen for patients with comorbidities or recent antibiotic use (described in the next section) should be given. (See 'Comorbidities, recent antibiotic use, or high rate of resistance' below and "Antibiotic studies for the treatment of community-acquired pneumonia in adults", section on 'Macrolide resistance' and "Resistance of Streptococcus pneumoniae to the macrolides, azalides, lincosamines, and ketolides", section on 'Macrolides and azalides' and "Resistance of Streptococcus pneumoniae to the fluoroquinolones, doxycycline, and trimethoprim-sulfamethoxazole", section on 'Doxycycline'.)

There is concern that widespread use of fluoroquinolones in outpatients will promote the development of fluoroquinolone resistance among respiratory pathogens (as well as other colonizing pathogens) and may lead to an increased incidence of C. difficile colitis [28]. In addition, empiric use of fluoroquinolones should not be used for patients at risk for Mycobacterium tuberculosis without an appropriate assessment for tuberculosis infection. The administration of a fluoroquinolone in patients with tuberculosis has been associated with a delay in diagnosis, increase in resistance, and poor outcomes. (See "Antibiotic studies for the treatment of community-acquired pneumonia in adults", section on 'Fluoroquinolone resistance' and "Clostridium difficile in adults: Epidemiology, microbiology, and pathophysiology", section on 'Antibiotic use'.)

Because of these concerns, the use of fluoroquinolones is discouraged in ambulatory patients with CAP without comorbid conditions or recent antimicrobial use, unless it is known that there is a high prevalence of macrolide-resistant S. pneumoniae in the local community.

Despite the caveats noted above about fluoroquinolones, these agents continue to be given, often inappropriately, for CAP. In one report of 768 ambulatory patients with CAP seen in an emergency department in 2000 and 2001, 245 (32 percent) were treated with levofloxacin; one-half of these patients did not meet the criteria for appropriate fluoroquinolone therapy [16].

Both the macrolides and the fluoroquinolones can cause a prolonged QT interval, which can result in torsades de pointes. Studies assessing the risk-benefit ratio of azithromycin are reviewed elsewhere (see "Azithromycin, clarithromycin, and telithromycin", section on 'QT interval prolongation and cardiovascular events'). For outpatients with known QT interval prolongation and for those considered to be at high risk of QT interval prolongation, we favor doxycycline since it has not been associated with QT interval prolongation. However, doxycycline should be avoided during pregnancy. It should also be noted that doxycycline has been less well studied for the treatment of CAP than the macrolides or fluoroquinolones. Risk factors for QT interval prolongation include advanced age, hypokalemia, hypomagnesemia, clinically significant bradycardia, and the use of other agents that prolong the QT interval, including class IA (quinidine, procainamide) and class III (dofetilide, amiodarone, sotalol) antiarrhythmic agents and certain azoles (eg, voriconazole, posaconazole). (See "Fluoroquinolones", section on 'QT interval prolongation and arrhythmia' and "Azithromycin, clarithromycin, and telithromycin", section on 'QT interval prolongation and cardiovascular events' and "Acquired long QT syndrome" and "Pharmacology of azoles", section on 'Selected clinical effects'.)


Content 2

Content 3








Content 2

Content 3




The approach to the patient with community-acquired pneumonia (CAP) begins with the clinical evaluation followed by chest radiograph with or without microbiologic testing [7].


RADIOLOGIC EVALUATION — The presence of an infiltrate on plain chest radiograph is considered the gold standard for diagnosing pneumonia when clinical and microbiologic features are supportive. A chest radiograph should be obtained in patients with suspected pneumonia when possible; a demonstrable infiltrate by chest radiograph or other imaging technique is required for the diagnosis of pneumonia, according to the 2007 consensus guidelines from the Infectious Diseases Society of America and the American Thoracic Society (IDSA/ATS) [4]. Recommendations are less clear in the patient with what appears to be a viral infection with nasal congestion and cough; one approach in these cases is to obtain a chest radiograph when there is an abnormal vital sign with particular emphasis on a respiratory rate >20 breaths/minute or a fever. This recommendation is relatively insensitive in older adult patients.

The radiographic appearance of community-acquired pneumonia (CAP) may include lobar consolidation (image 1 and image 2), interstitial infiltrates (image 3 and image 4 and image 5), and/or cavitation (image 6). It has been taught that lobar consolidation is due to the "typical" bacteria, and interstitial infiltrates are due to Pneumocystis jirovecii (formerly P. carinii) and viruses. However, radiologists cannot reliably differentiate bacterial from nonbacterial pneumonia on the basis of the radiographic appearance [9,11]. There is also substantial interobserver variation in the interpretation of chest radiographs in patients with possible pneumonia between different radiologists [12,13] and between emergency room physicians and radiologists [14]. It is also clear that high-resolution computed tomography (CT) is superior to chest radiography in detecting lesions and defining anatomical changes [15-17]. Nevertheless, chest radiograph (posteroanterior and lateral) is generally adequate for clinical care of most patients with CAP.

If the clinical evaluation does not support pneumonia in a patient with an abnormal chest radiograph, other causes for the radiographic abnormalities must be considered, such as malignancy, hemorrhage, pulmonary edema, pulmonary embolism, and inflammation secondary to noninfectious causes. On the other hand, if the clinical syndrome favors pneumonia but the radiograph is negative, the radiograph may represent a false-negative result. In some cases, this can be clarified with a CT scan, which, as noted above, has higher sensitivity and accuracy than chest radiographs for detecting CAP [15].

There are case reports and animal experiments favoring the hypothesis that volume depletion may produce an initially negative radiograph, which "blossoms" into infiltrates following rehydration [18]. In support of this hypothesis, one population-based cohort study of suspected CAP found that 7 percent of patients with negative initial radiographs developed changes consistent with CAP on repeat chest radiograph [19].

For hospitalized patients with suspected pneumonia and a negative chest radiograph, the 2007 IDSA/ATS consensus guidelines consider it reasonable to initiate empiric presumptive antibiotic therapy and repeat the chest radiograph in 24 to 48 hours [4]. The basis for this recommendation is from the classic studies of pneumococcal pneumonia, which found that the absence of infiltrate at 24 hours after onset of symptoms indicated the diagnosis needed to be questioned [20]. Alternatively, a CT scan could be performed in patients with a negative chest radiograph when there is a high clinical suspicion for pneumonia. CT scan, especially high-resolution CT (HRCT), is more sensitive than plain films for the evaluation of interstitial disease, bilateral disease, cavitation, empyema, and hilar adenopathy [15,21].

CT scanning is not generally recommended for routine use because the data for its use in CAP are limited, the cost is high, and there is no evidence that it improves outcome. Thus, a chest radiograph is the preferred method for initial imaging, with CT scan or magnetic resonance imaging (MRI) reserved for further anatomical definition (eg, detecting cavitation, adenopathy, or mass lesions).


Content 2

Pneumonia is acquired in healthcare facilities such as nursing homes, hemodialysis centers and outpatient clinics.


[The rationale to separate designation was that patients with HCAP were at higher risk for multidrug-resistant (MDR) organisms. However, several studies have shown that many patients defined as having HCAP are not at high risk for MDR pathogens [1-3]. Furthermore, although interaction with the healthcare system is potentially a risk for MDR pathogens, underlying patient characteristics are also important independent determinants of risk for MDR pathogens.]

Community Acquired

Treatment for pneumonia depends on the

type of pneumonia

how severe it is, and if you have other chronic diseases.



Most people can be treated at home by following these steps:

  • Drink plenty of fluids to help loosen secretions and bring up phlegm.
  • Get lots of rest. Have someone else do household chores.
  • Do not take cough medicines without first talking to your doctor. Cough medicines may make it harder for your body to cough up the extra sputum.
  • Control your fever with aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs, such as ibuprofen or naproxen), or acetaminophen. DO NOT give aspirin to children.


If your pneumonia becomes so severe that you are treated in the hospital, you may receive fluids and antibiotics in your veins, oxygen therapy, and possibly breathing treatments.

You are more likely to be admitted to the hospital if you:

  • Have another serious medical problem
  • Have severe symptoms
  • Are unable to care for yourself at home, or are unable to eat or drink
  • Are older than 65 or a young child
  • Have been taking antibiotics at home and are not getting better

Viral Pneumonia

use antiviral medication.  Viral pneumonia usually improves in 1 to 3 weeks.

Bacterial Pneumonia

Patients with mild pneumonia who are otherwise healthy are sometimes treated with oral macrolide antibiotics (azithromycin, clarithromycin, or erythromycin). Patients with other serious illnesses, such as heart disease, chronic obstructive pulmonary disease, or emphysema, kidney disease, or diabetes are often given more powerful or higher dose antibiotics.

In addition to antibiotics, treatment includes: proper diet and oxygen to increase oxygen in the blood when needed. In some patients, medication to ease chest pain and to provide relief from violent cough may be necessary.


A healthy young person may lead a normal life within a week of recovery from pneumonia. For middle-aged people, it may be weeks before they regain their usual strength and feeling of well-being.

A person recovering from mycoplasma pneumonia may be weak for an extended period of time. Adequate rest is important to maintain progress toward full recovery and to avoid relapse. Don't rush recovery!

[mild activty better for recovery]

Adjunctive glucocorticoids for adults with severe community-acquired pneumonia (Grade 2B)

Indication: Hospitalized adults with community-acquired pneumonia (CAP) who are at substantial risk of morbidity and mortality (eg, Pneumonia Severity Index score IV or V; CURB-65 score ≥2), with the proviso to less likely to give glucocorticoids to patients at increased risk of adverse effects.1

Glucocorticoids as adjunctive therapy to antibiotics have the potential to reduce the inflammatory response and decrease morbidity.

Reference Study: A 2015 meta-analysis of randomized trials that included hospitalized patients with CAP suggested a modest mortality benefit for adjunctive glucocorticoids [1]. A reduction in all-cause mortality was of borderline statistical significance (relative risk [RR] 0.67, 95% CI 0.45-1.01; risk difference 2.8 percent). Rates of mechanical ventilation and acute respiratory distress syndrome were decreased, as were time to clinical stability and duration of hospitalization; rates of hyperglycemia requiring treatment increased.

Decision whether or not to give glucocorticoids on a case-by-case basis, especially in patients with an elevated risk of adverse effects. Limited evidence suggests that infections caused by certain pathogens (eg, influenza virus, Aspergillus spp) may be associated with worse outcomes in the setting of glucocorticoid use [2,3]; given these concerns, we avoid adjunctive glucocorticoids if one of these pathogens is detected.


Antibiotic therapy is the cornerstone of medical management for community-acquired pneumonia.


To assess the associations between 3 key aspects of antibiotic therapy (optimal time to antibiotic initiation, initial antibiotic selection, and criteria for the transition from intravenous to oral therapy) and short-term mortality in adults hospitalized with community-acquired pneumonia.


Bibliographic databases of MEDLINE, EMBASE, and the Cochrane Collaboration were searched for studies of adults hospitalized with radiographically confirmed community-acquired pneumonia published from January 1, 1995, until November 5, 2015.


Twenty studies (17 observational and 3 randomized trials) met eligibility criteria. Among 8 observational studies identified, the 4 largest (study populations of 2878 to 1 170 022) found that antibiotic initiation within 4 to 8 hours of hospital arrival was associated with relative reductions of 5% to 43% in mortality; the 4 smallest studies (study populations of 451 to 2076) found no associations between the timing of antibiotic initiation and mortality. One cluster randomized trial (n = 1737) demonstrated noninferiority of β-lactam monotherapy (n = 506) vs β-lactam plus macrolide combination therapy (n = 566), with an absolute adjusted difference of 2.5% (90% CI, −0.6% to 5.2%) in 90-day mortality favoring β-lactam monotherapy. A second randomized trial (n = 580) failed to demonstrate noninferiority of β-lactam monotherapy vs β-lactam plus macrolide combination therapy, with an absolute difference of 7.6% (1-sided 90% CI upper limit, 13.0%) in attainment of clinical stability on hospital day 7 favoring β-lactam plus macrolide combination therapy. Six of 8 observational studies (study populations of 1188 to 24 780) found that β-lactam plus macrolide combination therapy was associated with relative reductions of 26% to 68% in short-term mortality and all 3 observational studies (study populations of 2068 to 24 780) reported that fluoroquinolone monotherapy was associated with relative reductions of 30% to 43% in mortality compared with β-lactam monotherapy. One randomized trial (n = 302) reported significantly reduced hospital length of stay (absolute difference, 1.9 days; 95% CI, 0.6 to 3.2 days), but no differences in treatment failure when objective clinical criteria were used to decide when to transition patients from intravenous to oral therapy.


In adults hospitalized with community-acquired pneumonia, antibiotic therapy consisting of β-lactam plus macrolide combination therapy or fluoroquinolone monotherapy initiated within 4 to 8 hours of hospital arrival was associated with lower adjusted short-term mortality, supported predominantly by low-quality observational studies. One randomized trial supports the use of objective clinical criteria to guide the transition from intravenous to oral antibiotic therapy.







Pneumonia is an infection that causes inflammation in one or both of the lungs and may be caused by a virus, bacteria, fungi or other germs (?).

It emanating from bacteria, viruses, fungi.and rarely parasites.1

When a person has pneumonia the air sacs in their lungs become filled with microorganisms, fluid and inflammatory cells and their lungs are not able to work properly. Diagnosis of pneumonia is based on symptoms and signs of an acute lower respiratory tract infection, and can be confirmed by a chest X‑ray showing new shadowing that is not due to any other cause (such as pulmonary oedema or infarction). In this guideline pneumonia is classified as community‑acquired or hospital‑acquired, based on different microbial causes and patient factors, which need different management strategies.


The goal when evaluating sputum in the laboratory is to confirm the diagnosis of pneumonia, identify the etiologic agent(s) responsible for producing the present disease, and guide selection of appropriate antibiotic therapy.



A video explanation of pneumonia


    • Arterial blood gases to see if enough oxygen is getting into your blood from the lungs
    • CT (or CAT) scan of the chest  to see how the lungs are functioning
    • Sputum tests to look for the organism (that can detected by studying your spit) causing your symptoms
    • Pleural fluid culture if there is fluid in the space surrounding the lungs
    • Pulse oximetry
    • Bronchoscopy



A diagram of the human body outlining the key symptoms of pneumonia

Diagnostic Criteria

 Chest X-ray, blood tests, and culture of the sputum may help confirm the diagnosis.[7] 

 Risk factors include other lung diseases such as cystic fibrosisCOPD, and asthma, diabetes, heart failure, a history of smoking, a poor ability to cough such as following a stroke, or a weak immune system.[6]


Pneumonia is usually caused by infection with viruses or bacteria and less commonly by other microorganisms, certain medications[??] and conditions such as autoimmune diseases.[2][5]

The disease may be classified by where it was acquired with community, hospital, or health care associated pneumonia.[8]


By Age

Viral Pathogens

Respiratory syncytial virus (RSV) is the most frequent cause of pneumonias in children with lower respiratory tract involvement (~50% cases) and is a particular problem in infants and young toddlers. RSV usually occurs in epidemics during the winter and early spring months, and infects virtually all children during the first 3 years of life. RSV is spread by direct or close contact with contaminated secretions or large infectious droplets in the air. Clinical features in RSV bronchiolitis include copious nasal discharge, cough, irritability, fever, and anorexia. Symptoms may progress over 3-7 days with worsening cough, dyspnea, and respiratory distress. Patients may develop significant tachypnea, nasal flaring, and sternal retractions. Wheezing is often a prominent feature that is accompanied by a prolonged expiratory phase. Underlying conditions that increase the risk of severe disease from RSV include children with congenital heart disease, immune deficiencies, or pulmonary disorders such as bronchopulmonary dysplasia (BPD).

RSV antigens in clinical specimens such as nasopharyngeal swabs are best detected using any of several rapid diagnostic tests that utilize immunofluorescent and enzyme immunoassay techniques. As with other viral causes of lower respiratory tract infection, treatment for RSV bronchiolitis includes adequate hydration, fever control, palliative measures, and supplemental oxygen in children who show hypoxemia. More aggressive therapeutic approaches have been proposed for RSV bronchiolitis, but lack evidence at present of their benefit in altering disease course, notably bronchodilators (albuterolepinephrine), corticosteroids, and the antiviral agent ribavirin. Clinicians have found that a patient's response to bronchodilators may change as the illness progresses, particularly in atopic children (eg, those with eczema) or in those with a strong family history of allergic disease. Prophylaxis against RSV infection in those infants at highest risk of severe disease is available in the form of a humanized monoclonal antibody that is directed against an RSV surface protein. Thus, palivizumab is approved for children <24 months of age who have BPD or a history of prematurity (<32 weeks' gestation). It is administered once monthly as an intramuscular injection during the high risk months of RSV disease (in North America, those being November through March).

In addition to RSV, other viruses and atypical organisms are capable of causing lower respiratory tract infections such as bronchiolitis or pneumonia. Parainfluenza viruses are second in frequency to RSV and cause ~25% of viral lower respiratory disease in this population, with type 3 the most likely to cause severe pneumonia. Parainfluenza infections can occur at any time of the year. Types 1 and 2 cause about one-third of all parainfluenza disease and are generally endemic in late summer and fall; type 3 tends to peak in the late spring and accounts for two-thirds of all parainfluenza cases. The parainfluenza viruses more typically cause upper respiratory tract disease, accounting for over half of the cases of laryngotracheitis (croup).

Adenoviruses cause 5%-7% of viral respiratory disease in children, often with a variety of syndromes that also affect the eyes, heart, bladder, and gastrointestinal tract. Adenoviral types 3, 4, 7, and 21 are associated with respiratory illnesses in children. Types 3, 7, and 21 have been identified in patients with severe adenoviral pneumonias and are linked to case fatality rates as high as 5%-10%. Residual adenovirus-caused morbidities can occur, notably bronchiectasisunilateral hyperlucent lung syndrome, bronchiolitis obliterans, or rarely, pulmonary fibrosis. Among the many viral etiologies of lower respiratory tract infections in children, adenoviral infections most often have features that are more usually identified with bacterial infections, such as lobar consolidations, pleural effusions, and high fevers.

Infections with influenza virus type A or type B cause another 5% of childhood respiratory illnesses. These are often accompanied by a variety of systemic symptoms including fever, headache, anorexia, malaise, myalgia, sore throat, vomiting, and abdominal pain. Respiratory complications from influenza may be limited to upper respiratory tract symptoms (croup, rhinitis), or the patient may present with pneumonia or a bronchiolitis-like illness. More so than in other viral infections, influenza infection is associated with an increased risk of secondary bacterial infections, particularly pneumonias due to S. aureus or S. pneumoniae.In this setting, the patient may improve clinically from the initial influenza illness but then have renewed fever, chills, cough, and respiratory distress, reflecting the bacterial superinfection. Treatment for routine influenza infections is supportive. In cases where more severe disease is a concern, antiviral agents can be administered provided this therapy is begun within 48 hours of the onset of symptoms.


Influenza viral infections occur in epidemics with a high attack rate lasting a relatively brief period of time. Influenza pandemics have led to millions of deaths worldwide in the past. The most dramatic example of this occurred in 1918, when an estimated 20 million people worldwide died. Outbreaks of influenza in the United States typically peak in the winter months with the highest attack rates in children. Influenza types A and B are the primary causes of epidemic disease worldwide and are further subdivided by distinct serotypes. Antigenic shift of these serotypes mandates changes in the composition of the annual influenza vaccine. The seasonal influenza vaccine is recommended for patients at high risk for severe complications from influenza (those with pulmonary or cardiac disorders) and in all children less than 5 years of age. Household contacts and caregivers of children with chronic disease should be vaccinated as well.

Metapneumovirus is a recently described pathogen (2001) which causes ~5% of lower respiratory tract disease, primarily in infants, but is reported in all age groups. Outbreaks occur in late winter and early spring in temperate climates and often coincide with the RSV season. Transmission probably occurs by direct contact with infected individuals, and nosocomial outbreaks have been described. Epidemiological studies point to metapneumovirus being the second leading cause of bronchiolitis in infants, after RSV. It causes pneumonia and croup in all age groups and is thought to be a major trigger of asthma exacerbations in children and adults. Clinical manifestations of metapneumovirus infection are similar to RSV disease with cough, wheeze, and respiratory distress being prominent features. More severe disease occurs in patients with congenital or acquired immune deficiencies, and likely those with underlying cardiopulmonary disorders and premature birth. Treatment for metapneumovirus, as with most viral lower respiratory tract infections, is supportive.

Mycoplasma pneumoniae is included with the discussion of viral pathogens since it is a frequent cause of "atypical" pneumonia, accounting for 5%-10% of respiratory tract infections in the pediatric population. Mycoplasmata are the smallest free-living microorganisms, lacking a cell wall. Pneumonia caused by M. pneumoniae is the prototype of the primary atypical pneumonia syndrome, although a variety of pathogens may be associated with this syndrome, including many described above. M. pneumoniae is the most common infectious agent causing pneumonia in older children and adolescents. It is a highly transmissible organism, with human to human spread by symptomatic individuals being a common cause of propagation within a family, school, military, or prison setting.

Initial symptoms in children with Mycoplasma pneumonia include malaise and fever. Cough may be an early symptom but typically arises or worsens later. Within a few days of the onset of illness a nonproductive cough develops with diffuse crackles often found on lung exam. Cough may become productive later in the illness and last up to four or more weeks. About 10% of children develop a maculopapular rash in the course of the illness. Radiographically, the typical pattern is bilateral diffuse infiltrates that may be particularly pronounced in the lower lobes. Definitive diagnosis of Mycoplasma disease relies on acute and convalescent sera utilizing complement fixation or immunofluorescent assays. A fourfold or greater increase in titer or the presence of specific IgM antibodies confirms recent infection. By the second week of illness, cold agglutinin titers of 1:32 or greater are present in half of patients with pneumonia. However, this test lacks specificity. Treatment with tetracyclines, or with macrolides such as erythromycin or newer derivatives (clarithromycinazithromycin) are effective in shortening the clinical manifestations of the disease.

Bacterial Pathogens

Streptococcus pneumoniae

S. pneumoniae (formerly Pneumococcus pneumoniae) is frequently detected in the upper respiratory tract of children. There it can cause disease including sinusitis or otitis media, or more invasively pneumonia,meningitis, or bacteremic sepsis. It is a common cause of community-acquired pneumonia in children, responsible for more than 50% of patients requiring hospital admission. The near-universal use of theheptavalent pneumococcal conjugate vaccine in the United States has had a substantial impact on the epidemiology of invasive pneumococcal disease. The incidence of invasive disease has dropped among vaccinated children, and upper respiratory tract colonization with this organism has fallen, but there has been a notable shift in pneumococcal serotypes causing disease in those not covered by the vaccine. As noted, the introduction of a conjugate vaccine protecting against 13 serotypes may have a broader impact on the incidence of pneumococcal disease (see Clinical Correlation 40.1). High-risk groups for invasive disease include Native American and African-Americanchildren, children with sickle cell disease, children with acquired or congenital splenic disorders, and children with HIV infection or otherimmune deficiencies.

Clinical manifestations of pneumococcal disease are protean, with most children presenting with spiking fevers, cough, an elevated leukocyte count, and lobar or segmental consolidation on chest radiographs. Notably, up to one-fourth of children may have no signs or symptoms attributable to respiratory tract disease and instead present with fever, abdominal pain, or diarrhea. Further, many different radiographic patterns have been described in pneumococcal pneumonia, above and beyond the typical lobar abnormalities (Fig. 40.2). Complications arising from pneumococcal pneumonia are not uncommon in hospitalized children and include parapneumonic effusionsempyemaabscess formation, and necrotizing pneumonia. Although antibiotic-resistant isolates are not predictive of these morbidities, patients with complicated pneumonias tend to be older, are more likely to be Caucasian, and more likely to present with chest pain. Provided that empiric antibiotic choices are correct, most patients will improve within 2-4 days. Ongoing fever, chills, chest or abdominal pain, or the lack of an improvement in the overall clinical picture should raise concerns for one of the above complications.

Pleural effusions accompanying pneumococcal chest infections are the result of a complicated pathophysiologic process (Chap. 29). Parenchymal lung injury causes an inflammatory response of the pleural surfaces and a subsequent increase in regional capillary permeability. This pleural inflammation also reduces the dynamic process of pleural fluid reabsorption by the parietal pleura. When this is combined with the change in capillary permeability, considerable amounts of fluid can accumulate. Initially, pleural effusions are sterile, free flowing, and contain fluid with few leukocytes. This exudative phase (or stage 1) may last for 3-5 days before giving way to the fibrinopurulent phase where an increase in leukocytes and a positive Gram stain indicative of infected fluid are observed (Chap. 19). With the development of pus in the pleural space, fibrin deposition between the visceral and parietal pleura ensues. The infected fluid accordingly becomes loculated, fibrin and cellular debris accumulate and more fluid becomes apparent as lymphatic channels become obstructed. The organizing stage (stage 3) is characterized by infiltration of fibroblasts, thickening of the pleural membranes and "trapped" lobes (Chap. 26).

In the initial stages of a pleural effusion, fluid removal is amenable to simple needle thoracentesis or via chest tube placement. This approach may be both diagnostic and therapeutic (Chap. 19). In the later stages, these approaches may not be successful as the loculated, purulent fluid may be difficult to drain. Video-assisted thoracoscopic surgery (VATS) to evacuate pleural fluid and perform decortications with debridement of thickened pleural membranes is a surgical option. On the other hand, some clinicians favor an approach of chest tube placement in conjunction with a fibrinolytic agent such as tissue plasminogen activator instilled into the chest tube (Chap. 27). Less frequently, continuing medical therapy with IV antibiotics alone to manage pneumonias with large effusions is an option. Though S. pneumoniae is the most common cause of pneumonias with effusions, other organisms such as Group A StreptococcusS. aureusH. influenzae, Pseudomonas aeruginosa, and Mycoplasma spp. can also cause complicated parapneumonic effusions.

The development of a pulmonary abscess is another complication of bacterial pneumonias, including those caused by S. pneumoniae. A lung abscess is a thick-walled cavity containing pus, leukocytes, and cellular debris. In some circumstances, it is the result of an aspiration event, especially in children with neurodevelopmental deficits. The clinical presentation of a pulmonary abscess mirrors that of children with typical bacterial pneumonias, with fever and cough being the prominent features. The course of illness may be subacute with a slower evolution of signs and symptoms. The chest radiograph shows a typical appearance of a fluid-filled cavity with an air-fluid level (Fig. 40.4). Chest ultrasound or CT scan may be an adjunct to diagnosis and guide possible drainage procedures. Most clinicians recommend IV antibiotics for up to 2 weeks with an additional 2-4 weeks of oral therapy. Newer information suggests that draining abscess fluid or placing a pigtail catheter in the cavity in conjunction with IV antibiotic therapy may shorten the hospital stay.


A PA x-ray of a previously healthy 7-year-old girl with cough, fever, and chest pain. A cavity with an air-fluid level is present in the left lung, indicative of a pulmonary abscess. A culture from a needle aspiration of this cavity was positive for S. pneumoniae.

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Other Bacterial Pathogens

H. influenzae type B was a frequent cause of significant bacterial disease among children in the past. Invasive diseases caused by H. influenzae type B include sepsis, meningitis, epiglottitis, cellulitis, and pneumonia. An effective vaccine to prevent disease caused by this organism became available in the late 1980s and resulted in a dramatic decrease in the incidence of these illnesses. Although H. influenzae type B is no longer a significant cause of bacterial pneumonia in affluent countries, the worldwide morbidity and mortality from this organism remains an important problem. Nearly 90% of children who develop infections with this pathogen are <5 years of age, and the majority of these are <2 years old. Pneumonias due to H. influenzae cannot be differentiated by clinical criteria from pneumonias caused by other bacteria. Radiographic findings vary, with pleural effusion a common finding. Because of the risk of systemic complications (bacteremia, meningitis) in children <12 months of age in whom H. influenzae is considered a likely pathogen, IV antibiotics should be administered. Older children who are at lower risk of developing these complications may be treated with oral therapy.

While not very common, the community-acquired pneumonia caused byGroup A Streptococcus (S. pyogenes) is often associated with a particularly protracted and difficult course in some children. Group AStreptococcus causes a variety of infections involving the upper respiratory tract and skin, but when it involves the lower respiratory tract, a diffuse infection with interstitial pneumonia may occur. In its severe form, necrosis of the airway mucosa and lung parenchyma takes place accompanied by hemorrhage, exudates, edema, and pleural involvement (Chap. 34). Previous infection with influenza virus, measles, or Varicella may place the patient at particular risk of developing severe complications of Group A Streptococcal disease.

In most cases of community-acquired pneumonia caused byStaphylococcus aureus, infection is either by direct inoculation of the organism into the respiratory tree or, less commonly, following bacteremic illness. Exceptions are those patients with indwelling catheters or a recent history of intravenous drug use, where the bacteremic route more commonly causes pneumonia (Chap. 28). Since most clinical protocols for treatment of community-acquired pneumonias do not include therapy directed against S. aureus, the clinical picture may be one of ongoing fever, cough, chills, and supplemental oxygen requirement. A subacute or acute deterioration in clinical status may be observed if this organism is not suspected. Radiographically, unilateral lung involvement is typical with confluent bronchopneumonia and alveolar infiltrates (Chap. 15). As the illness evolves, these areas may coalesce and cavitate, leading to the formation of pneumatoceles. In a large proportion of patients whose pneumonia is caused by S. aureus, complicated parapneumonic effusions and empyema develop. More severely in some patients, a pyopneumothorax may occur characterized by both pus and air in the pleural space. With the increasing prevalence of methicillin-resistant S. aureus (MRSA) in the United States and elsewhere, antibiotic therapy may need to be adjusted to account for this organism, depending on local microbiologic surveillance data.




1. Community-Acquired Pneumonia

a. Determine if patient can be manage as an outpatient using CRB-65 Criteria.

> NEXT: 02. CRB 65 SCALE


Complications of Injecting Drug Use

  • Local problems—Abscess (Figures 240-2 
    Image not available.

    A 32-year-old woman with type 1 diabetes developed large abscesses all over her body secondary to injection of cocaine and heroin. Her back shows the large scars remaining after the healing of these abscesses. (Courtesy of ­Richard P. Usatine, MD.)

    and 240-3; Abscess), cellulitis, septic thrombophlebitis, local induration, necrotizing fasciitis, gas gangrene, pyomyositis, mycotic aneurysm, compartmental syndromes, and foreign bodies (e.g., broken needle parts) in local areas.2
    • IDUs are at higher risk of getting methicillin-resistant Staphylococcus aureus(MRSA) skin infections that the patient may think are spider bites (Figure 240-4).
    • Some IDUs give up trying to inject into their veins and put the cocaine directly into the skin. This causes local skin necrosis that produces round atrophic scars (Figure 240-5).
  • IDUs are at risk for contracting systemic infections, including HIV and hepatitis B or hepatitis C.
    • Injecting drug users are at risk of endocarditis, osteomyelitis (Figures 240-6and 240-7), and an abscess of the epidural region. These infections can lead to long hospitalizations for intravenous antibiotics. The endocarditis that occurs in IDUs involves the right-sided heart valves (see Chapter 50, Bacterial Endocarditis).2 They are also at risk of septic emboli to the lungs, group A β-hemolytic streptococcal septicemia, septic arthritis, and candidal and other fungal infections.


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Content 13

A 68-year-old man presents to the hospital emergency department with acute fever and persistent cough.

He has had cough productive of green sputum for 3 days, associated with shortness of breath, left-sided pleuritic chest pain, fever, chills, and night sweats.

His medical history is notable for chronic obstructive pulmonary disease (COPD), requiring intermittent oral glucocorticoid use. His medications include albuterolipratropium bromide, and corticosteroid inhalers. The patient lives at home and is active. On examination, he is febrile to 38°C, with a blood pressure of 110/50 mm Hg, heart rate of 98 bpm, and respiratory rate of 20/min. Oxygen saturation is 92% on room air. He is a thin man in moderate respiratory distress, speaking in sentences of three or four words. Lung examination is notable for rales in the left lung base and left axilla and diffuse expiratory wheezes. The remainder of the examination is unremarkable. Chest x-ray film reveals left lower lobe and lingular infiltrates. A diagnosis of pneumonia is made, and the patient is admitted to the hospital for administration of intravenous antibiotics.


A 31-year-old woman presents to the emergency room with the acute onset of malaise, fever, and a productive cough. A chest x-ray reveals consolidation of the right lower lobe along with air bronchograms, and a Gram stain of her sputum shows a predominance of gram-positive lancet-shaped cocci in pairs and chains. Which of the following is the most likely causative agent of this individual's infectious disease?

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The correct answer is D. You answered B.

D. Although infection of the lung parenchyma (pneumonia) can be caused by a number of different types of organisms, most commonly pneumonia results from bacterial infection (bacterial pneumonia) of the lung. There are two basic patterns of bacterial pneumonia: lobar pneumonia, which is characterized by involvement of an entire lobe by a virulent organism, and lobular pneumonia (bronchopneumonia), which is characterized by patchy inflammation involving one or more lobes. The vast majority of cases of lobar pneumonia, which is the more common type of bacterial pneumonia, are caused by infection with Streptococcus pneumoniae. With pneumococcal pneumonia, patients usually present with fever, a productive cough with rust-colored sputum, and pleuritic chest pain.


A 75-year-old triathlete complains of gradually worsening vision over the past year. It seems to be involving near and far vision. The patient has never required corrective lenses and has no significant medical history other than diet-controlled hypertension. He takes no regular medications. Physical examination is normal except for bilateral visual acuity of 20/100. There are no focal visual field defects and no redness of the eyes or eyelids. Which of the following is the most likely diagnosis?

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The correct answer is A. You answered A.

Age-related macular degeneration is a major cause of painless, gradual bilateral central visual loss. It occurs as nonexudative (dry) or exudative (wet) forms. Recent genetic data have shown an association with the alternative complement pathway gene for complement factor H. The mechanism link for that association is unknown. The nonexudative form is associated with retinal drusen that leads to retinal atrophy. Treatment with vitamin C, vitamin E, beta-carotene, and zinc may retard the visual loss. Exudative macular degeneration, which is less common, is caused by neovascular proliferation and leakage of choroidal blood vessels. Acute visual loss may occur because of bleeding. Exudative macular degeneration may be treated with intraocular injection of a vascular endothelial growth factor antagonist (bevacizumab or ranibizumab). Blepharitis is inflammation of the eyelids usually related to acne rosacea, seborrheic dermatitis, or staphylococcal infection. Diabetic retinopathy, now a leading cause of blindness in the United States, causes gradual bilateral visual loss in patients with long-standing diabetes. Retinal detachment is usually unilateral and causes visual loss and an afferent pupillary defect.


Mr. Jenson is a 40-year-old man with a congenital bicuspid aortic valve who you have been seeing for more than a decade. You obtain an echocardiogram every other year to follow the progression of his disease knowing that bicuspid valves often develop stenosis or regurgitation requiring replacement in middle age. Given his specific congenital abnormality, what other anatomic structure is important to follow on his biannual echocardiograms?

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The correct answer is A. You answered A.

The answer is A. (Chap. 282) Bicuspid aortic valve is among the most common of congenital heart cardiac abnormalities. Valvular function is often normal in early life and thus may escape detection. Due to abnormal flow dynamics through the bicuspid aortic valve, the valve leaflets can become rigid and fibrosed, leading to either stenosis or regurgitation. However, pathology in patients with bicuspid aortic valve is not limited to the valve alone. The ascending aorta is often dilated, misnamed “poststenotic” dilatation; this is due to histologic abnormalities of the aortic media and may result in aortic dissection. It is important to screen specifically for aortopathy because dissection is a common cause of sudden death in these patients.