Pneumonia: Causes, symptoms and management

Community-Acquired Pneumonia

Community-Acquired Pneumonia

Pneumonia is a type of lung infection. It can cause breathing problems and other symptoms. In community-acquired pneumonia (CAP), you get infected in a community setting. It doesn’t happen in a hospital, nursing home, or other healthcare center.

Your lungs are part of your respiratory system. This system supplies fresh oxygen to your blood and removes carbon dioxide, a waste product. When you breathe in air through your nose and mouth, it reaches the tiny air sacs of the lung (alveoli) through a series of tubes. From here, oxygen flows into your blood. Carbon dioxide flows out from the blood into the alveoli and you then breathe it out.

Many germs can grow inside your body and cause disease. Specific types of germs can cause lung infection and pneumonia when they invade. This can cause your respiratory system to work poorly. For example, oxygen may not be able to get into your blood as easily. That can cause shortness of breath. If your body can’t get enough oxygen to survive, pneumonia may lead to death.

Sometimes these germs can spread from person to person. When someone infected with one of these germs sneezes or coughs, you might breathe the germs into your lungs. If your immune system doesn’t kill the germs first, the germs might grow and cause pneumonia.

Community-acquired pneumonia (CAP) is a common disorder, with approximately 4–5 million cases diagnosed each year in the United States, 25% of which require hospitalization. It is the deadliest infectious disease in the United States and the eighth leading cause of death. Mortality in milder cases treated as outpatients is less than 1%. Among patients hospitalized for CAP, in-hospital mortality is approximately 10–12% and 1-year mortality (in those over age 65) is greater than 40%.

Risk factors for the development of CAP include advanced age; alcoholism; tobacco use; comorbid medical conditions, especially asthma or COPD; and immunosuppression.


Many different types of germs can cause pneumonia. But certain types cause CAP more often. Worldwide, Streptococcus pneumoniae is a bacteria that is most often responsible for CAP in adults. Some other common bacteria that cause CAP are:

  • Haemophilus influenzae
  • Mycoplasma pneumoniae
  • Chlamydia pneumoniae
  • Legionella
  • Gram-negative bacilli
  • Staphylococcus aureus

The flu (influenza) virus is the major viral cause of CAP. Having the flu also makes you more likely to get bacterial pneumonia. This type is often worse than viral pneumonia. Other types of viruses can also cause CAP, such as parainfluenza virus, echovirus, adenovirus, and coxsackievirus. In fact, viruses are likely responsible for most episodes of CAP. Fungi and parasites may also cause CAP


The patient’s history, physical examination, and imaging studies are essential to establishing a diagnosis of CAP. None of these efforts identifies a specific microbiologic cause, however. Sputum examination may be helpful in selected patients but 40% of patients cannot produce an evaluable sputum sample and Gram stain and culture lack sensitivity for the most common causes of pneumonia.

Since patient outcomes improve when the initial antibiotic choice is appropriate for the infecting organism, the American Thoracic Society and the Infectious Diseases Society of America recommend empiric treatment based on epidemiologic data. Such treatment improves initial antibiotic coverage, reduces unnecessary hospitalization, and appears to improve 30-day survival.

CAP is diagnosed outside of the hospital in ambulatory patients who are not residents of nursing homes or other long-term care facilities. It may also be diagnosed in a previously ambulatory patient within 48 hours after admission to the hospital.

Pulmonary defense mechanisms (cough reflex, mucociliary clearance system, immune responses) normally prevent the development of lower respiratory tract infections following aspiration of oropharyngeal secretions containing bacteria or inhalation of infected aerosols. CAP occurs when there is a defect in one or more of these normal defense mechanisms or when a large infectious inoculum or a virulent pathogen overwhelms the immune response.


A pulmonary opacity on chest radiography or CT scan is required to establish a diagnosis of CAP. Chest CT scan is more sensitive and specific than chest radiography and may be indicated in selected cases.

Radiographic findings range from patchy airspace opacities to lobar consolidation with air bronchograms to diffuse alveolar or interstitial opacities.

Additional findings can include pleural effusions and cavitation. Chest imaging cannot identify a specific microbiologic cause of CAP, however. No pattern of radiographic abnormalities is pathognomonic of any infectious cause.

Chest imaging may help assess severity and response to therapy over time. Progression of pulmonary opacities during antibiotic therapy or lack of radiographic improvement over time are poor prognostic signs and also raise concerns about secondary or alternative pulmonary processes. Clearing of pulmonary opacities in patients with CAP can take 6 weeks or longer. Clearance is usually quickest in younger patients, nonsmokers, and those with only single-lobe involvement.

Special Examinations

Patients with CAP who have significant pleural fluid collections may require diagnostic thoracentesis (glucose, lactate dehydrogenase [LD], and total protein levels; leukocyte count with differential; pH determination) with pleural fluid Gram stain and culture. Positive pleural cultures indicate the need for tube thoracostomy drainage.

Patients with cavitary opacities should have sputum fungal and mycobacterial cultures.

Sputum induction and fiberoptic bronchoscopy to obtain samples of lower respiratory secretions are indicated in patients who cannot provide expectorated sputum samples or who may have P jirovecii or M tuberculosis pneumonia.

Serologic assays, polymerase chain reaction tests, specialized culture tests, and other diagnostic tests for organisms such as viruses, Legionella, M pneumoniae, and C pneumoniae may be performed when these diagnoses are suspected.

Differential Diagnosis

The differential diagnosis of lower respiratory tract infection is extensive and includes upper respiratory tract infections, reactive airway diseases, heart failure, cryptogenic organizing pneumonitis, lung cancer, pulmonary vasculitis, pulmonary thromboembolic disease, and atelectasis.

Symptoms and Signs

Most patients with CAP experience an acute or subacute onset of fever, cough with or without sputum production, and dyspnea. Other common symptoms include sweats, chills, rigors, chest discomfort, pleurisy, hemoptysis, fatigue, myalgias, anorexia, headache, and abdominal pain.

Common physical findings include fever or hypothermia, tachypnea, tachycardia, and arterial oxygen desaturation. Many patients appear acutely ill. Chest examination often reveals inspiratory crackles and bronchial breath sounds. Dullness to percussion may be observed if lobar consolidation or a parapneumonic pleural effusion is present. The clinical evaluation is less than 50% sensitive compared to chest imaging for the diagnosis of CAP. In most patients, therefore, a chest radiograph is essential to the evaluation of suspected CAP.


Two general principles guide antibiotic therapy once the diagnosis of CAP is established: prompt initiation of a medication to which the etiologic pathogen is susceptible.

In patients who require specific diagnostic evaluation, sputum and blood culture specimens should be obtained prior to initiation of antibiotics. Since early administration of antibiotics to acutely ill patients is associated with improved outcomes, obtaining other diagnostic specimens or test results should not delay the initial dose of antibiotics.

Optimal antibiotic therapy would be pathogen directed, but a definitive microbiologic diagnosis is rarely available on or within 6 hours of presentation. A syndromic approach to therapy, based on clinical presentation and chest imaging, does not reliably predict the microbiology of CAP. Therefore, initial antibiotic choices are typically empiric, based on acuity (treatment as an outpatient, inpatient, or in the ICU), patient risk factors for specific pathogens, and local antibiotic resistance patterns.

Since S pneumoniae remains a common cause of CAP in all patient groups, local prevalence of drug-resistant S pneumoniae significantly affects initial antibiotic choice. Prior treatment with one antibiotic in a pharmacologic class (eg, beta-lactam, macrolide, fluoroquinolone) predisposes the emergence of drug-resistant S pneumoniae, with resistance developing against that class of antibiotics to which the pathogen was previously exposed. Definitions of resistance have shifted based on observations of continued clinical efficacy at achievable serum levels.

In CAP, for parenteral penicillin G or oral amoxicillin, susceptible strains have a minimum inhibitory concentration (MIC) 2 mcg/mL or less; intermediate resistance is defined as an MIC between 2 mcg/mL and 4 mcg/mL because treatment failures are uncommon with MIC 4 mcg/mL or less. Macrolide resistance has increased; approximately one-third of S pneumoniae isolates now show in vitro resistance to macrolides.

Treatment failures have been reported but remain rare compared to the number of patients treated; current in vivo efficacy appears to justify maintaining macrolides as first-line therapy except in areas where there is a high prevalence of resistant strains. S pneumoniae resistant to fluoroquinolones is rare in the United States (1% to levofloxacin, 2% to ciprofloxacin) but is increasing.

Community-acquired methicillin-resistant S aureus (CA-MRSA) is genetically and phenotypically different from hospital-acquired MRSA strains. CA-MRSA is a rare cause of necrotizing pneumonia, empyema, respiratory failure, and shock; it appears to be associated with prior influenza infection. Linezolid may be preferred to vancomycin in treatment of CA-MRSA pulmonary infection. F

Recommended empiric antibiotics for community-acquired pneumonia.

Outpatient management

  1. For previously healthy patients who have not taken antibiotics within the past 3 months: a. A macrolide (clarithromycin, 500 mg orally twice a day; or azithromycin, 500 mg orally as a first dose and then 250 mg orally daily for 4 days, or 500 mg orally daily for 3 days), or b. Doxycycline, 100 mg orally twice a day.
  2. For patients with comorbid medical conditions such as chronic heart, lung, liver, or kidney disease; diabetes mellitus; alcoholism; malignancy; asplenia; immunosuppressant conditions or use of immunosuppressive drugs; or use of antibiotics within the previous 3 months (in which case an alternative from a different antibiotic class should be selected): a. A respiratory fluoroquinolone (moxifloxacin, 400 mg orally daily; gemifloxacin, 320 mg orally daily; levofloxacin, 750 mg orally daily) or b. A macrolide (as above) plus a beta-lactam (amoxicillin, 1 g orally three times a day; amoxicillin-clavulanate, 2 g orally twice a day are preferred to cefpodoxime, 200 mg orally twice a day; cefuroxime, 500 mg orally twice a day).
  3. In regions with a high rate (> 25%) of infection with high level (MIC ≥ 16 mcg/mL) macrolide-resistant Streptococcus pneumoniae, consider use of alternative agents listed above in (2) for patients with comorbidities

Inpatient management not requiring intensive care

  1. A respiratory fluoroquinolone. See above for oral therapy. For intravenous therapy, moxifloxacin, 400 mg daily; levofloxacin, 750 mg daily; ciprofloxacin, 400 mg every 8–12 hours, or
  2. A macrolide plus a beta-lactam. See above for oral therapy. For intravenous therapy, ampicillin, 1–2 g every 4–6 hours; cefotaxime, 1–2 g every 4–12 hours; ceftriaxone, 1–2 g every 12–24 hours.

Inpatient intravenous management requiring intensive care

  1. Azithromycin (500 mg orally as a first dose and then 250 mg orally daily for 4 days, or 500 mg orally daily for 3 days) or a respiratory fluoroquinolone plus an antipneumococcal beta-lactam (cefotaxime, ceftriaxone, or ampicillin-sulbactam, 1.5–3 g every 6 hours).
  2. For patients allergic to beta-lactam antibiotics, a fluoroquinolone plus aztreonam (1–2 g every 6–12 hours).
  3. For patients at risk for Pseudomonas infection: a. An antipneumococcal, antipseudomonal beta-lactam (piperacillin-tazobactam, 3.375–4.5 g every 6 hours; cefepime, 1–2 g twice a day; imipenem, 0.5–1 g every 6–8 hours; meropenem, 1 g every 8 hours) plus ciprofloxacin (400 mg every 8–12 hours) or levofloxacin, or b. The above beta-lactam plus an aminoglycoside (gentamicin, tobramycin, amikacin, all weight-based dosing administered daily adjusted to appropriate trough levels) plus azithromycin or a respiratory fluoroquinolone.
  4. For patients at risk for methicillin-resistant Staphylococcus aureus infection, add vancomycin (interval dosing based on kidney function to achieve serum trough concentration 15–20 mcg/mL) or linezolid (600 mg twice a day).

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