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Community-acquired pneumonia develops in people with limited or no contact with medical institutions or settings. The most commonly identified pathogens are Streptococcus pneumoniae, Haemophilus influenzae, atypical bacteria (ie, Chlamydia pneumoniae, Mycoplasma pneumoniae, Legionella sp), and viruses. Symptoms and signs are fever, cough, sputum production, pleuritic chest pain, dyspnea, tachypnea, and tachycardia. Diagnosis is based on clinical presentation and chest x-ray. Treatment is with empirically chosen antibiotics. Prognosis is excellent for relatively young or healthy patients, but many pneumonias, especially when caused by S. pneumoniae, Legionella, Staphylococcus aureus, or influenza virus, are serious or even fatal in older, sicker patients.
Many organisms cause community-acquired pneumonia, including bacteria, viruses, and fungi. Pathogens vary by patient age and other factors (see Table: Community-Acquired Pneumonia in Adults), but the relative importance of each as a cause of community-acquired pneumonia is uncertain, because most patients do not undergo thorough testing, and because even with testing, specific agents are identified in < 50% of cases (see Overview of Pneumonia ).
S. pneumoniae, H. influenzae, C. pneumoniae, and M. pneumoniaeare the most common bacterial causes. Pneumonias caused by chlamydia and mycoplasma are often clinically indistinguishable from other pneumonias. Common viral agents include respiratory syncytial virus (RSV), adenovirus, influenza viruses, metapneumovirus, and parainfluenza viruses. Bacterial superinfection can make distinguishing viral from bacterial infection difficult.
C. pneumoniae accounts for 2 to 5% of community-acquired pneumonia and is the 2nd most common cause of lung infections in healthy people aged 5 to 35 yr. C. pneumoniae is commonly responsible for outbreaks of respiratory infection within families, in college dormitories, and in military training camps. It causes a relatively benign form of pneumonia that infrequently requires hospitalization. Chlamydia psittaci pneumonia (psittacosis) is rare and occurs in patients who own or are often exposed to birds.
Since the year 2000, the incidence of community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) skin infections has increased markedly. This pathogen can rarely cause severe, cavitating pneumonia and tends to affect young adults.
P. aeruginosa is an especially common cause of pneumonia in patients with cystic fibrosis, neutropenia, advanced AIDS, and/or bronchiectasis.
A host of other organisms causes lung infection in immunocompetent patients. In patients with pneumonia, a thorough history of exposures, travel, pets, hobbies, and other exposures is essential to raise suspicion of less common organisms.
Q fever, tularemia, anthrax, and plague are uncommon bacterial syndromes in which pneumonia may be a prominent feature. Tularemia (see Tularemia ), anthrax (see Anthrax ), and plague (see Plague and Other Yersinia Infections ) should raise the suspicion of bioterrorism (see Biological Agents as Weapons ).
Adenovirus, Epstein-Barr virus, and coxsackievirus are common viruses that rarely cause pneumonia. Seasonal influenza can rarely cause a direct viral pneumonia but often predisposes to the development of a serious secondary bacterial pneumonia. Varicella virus and hantavirus cause lung infection as part of adult chickenpox and hantavirus pulmonary syndrome. A coronavirus causes severe acute respiratory syndrome (SARS) and the Middle East Respiratory syndrome (MERS—see Coronaviruses and Acute Respiratory Syndromes (MERS and SARS) ).
Common fungal pathogens include Histoplasma capsulatum (histoplasmosis—see Histoplasmosis ) and Coccidioides immitis (coccidioidomycosis—see Coccidioidomycosis ). Less common fungal pathogens include Blastomyces dermatitidis (blastomycosis—see Blastomycosis ) and Paracoccidioides braziliensis (paracoccidioidomycosis—see Paracoccidioidomycosis ). Pneumocystis jirovecii commonly causes pneumonia in patients who have HIV infection or are immunosuppressed (see Pneumonia in Immunocompromised Patients ).
Parasites causing lung infection in developed countries include Toxocara canis or T. catis (visceral larva migrans—see Toxocariasis ), Dirofilaria immitis (dirofilariasis—see Dirofilariasis ), and Paragonimus westermani (paragonimiasis—see Paragonimiasis ). (For a discussion of pulmonary TB or of specific microorganisms, see Mycobacteria .)
In children, the most common causes depend on age:
S. pneumoniae and MRSA can cause necrotizing pneumonia.
For pneumonia in neonates, see Neonatal Pneumonia .
Symptoms include malaise, chills, rigor, fever, cough, dyspnea, and chest pain. Cough typically is productive in older children and adults and dry in infants, young children, and the elderly. Dyspnea usually is mild and exertional and is rarely present at rest. Chest pain is pleuritic and is adjacent to the infected area. Pneumonia may manifest as upper abdominal pain when lower lobe infection irritates the diaphragm. GI symptoms (nausea, vomiting, diarrhea) are also common. Symptoms become variable at the extremes of age. Infection in infants may manifest as nonspecific irritability and restlessness; in the elderly, as confusion and obtundation.
Signs include fever, tachypnea, tachycardia, crackles, bronchial breath sounds, egophony (E to A change—said to occur when, during auscultation, a patient says the letter “E” and the examiner hears the letter “A”), and dullness to percussion. Signs of pleural effusion may also be present (see Pleural Effusion : Symptoms and Signs). Nasal flaring, use of accessory muscles, and cyanosis are common among infants. Fever is frequently absent in the elderly.
Symptoms and signs were previously thought to differ by type of pathogen. For example, factors thought to suggest viral pneumonia included gradual onset, preceding URI symptoms, diffuse findings on auscultation, and absence of a toxic appearance. Atypical pathogens were considered more likely when onset was less acute and are more likely during known community outbreaks. However, manifestations in patients with typical and atypical pathogens overlap considerably. In addition, no single symptom or sign is sensitive or specific enough to predict the organism. Symptoms and signs are even similar for other noninfective inflammatory lung diseases such as hypersensitivity pneumonitis and organizing pneumonia.
Diagnosis is suspected on the basis of clinical presentation and infiltrate seen on chest x-ray. When there is high clinical suspicion of pneumonia and the chest x-ray does not reveal an infiltrate, doing CT or repeating the chest x-ray in 24 to 48 h is recommended.
Differential diagnosis in patients presenting with pneumonia-like symptoms includes heart failure (see Heart Failure ) and COPD exacerbation (see Chronic Obstructive Pulmonary Disease (COPD) ). Other disorders should be considered, particularly when findings are inconsistent or not typical. The most serious common misdiagnosis is pulmonary embolism, which may be more likely in patients with minimal sputum production, no accompanying URI or systemic symptoms, and risk factors for thromboembolism (see Table: Risk Factors for Deep Venous Thrombosis and Pulmonary Embolism); thus, testing for pulmonary embolism should be considered. Quantitative cultures of bronchoscopic or suctioned specimens, if they are obtained before antibiotic administration, can help distinguish between bacterial colonization (ie, presence of microorganisms at levels that provoke neither symptoms nor an immune response) and infection. However, bronchoscopy is usually done only in patients receiving mechanical ventilation or for those with other risk factors for unusual microorganisms or complicated pneumonia (eg, immunocompromise, failure of empiric therapy).
Distinguishing between bacterial and viral pneumonias is challenging. Many studies have investigated the utility of clinical, imaging, and routine blood tests, but no test is reliable enough to make this differentiation. The use of serum biomarkers, such as procalcitonin and C-reactive protein (CRP), to help in differentiating bacterial from nonbacterial pneumonia is currently under investigation.
In outpatients with mild or moderate pneumonia, no further diagnostic testing is needed (see Table: Risk Stratification for Community-Acquired Pneumonia (the Pneumonia Severity Index)). In patients with moderate or severe pneumonia, a WBC count and electrolytes, BUN, and creatinine are useful to classify risk and hydration status. Pulse oximetry or ABG testing should also be done to assess oxygenation. For patients with moderate or severe pneumonia who require hospitalization, 2 sets of blood cultures are obtained to assess for bacteremia and sepsis. The IDSA provides a guide to recommended testing based on patient demographic and risk factors ( Infectious Diseases Society of America Clinical Guideline on Community-Acquired Pneumonia ).
Identification of the pathogen can be useful to direct therapy and verify bacterial susceptibilities to antibiotics. However, because of the limitations of current diagnostic tests and the success of empiric antibiotic treatment, experts recommend limiting attempts at microbiologic identification (eg, cultures, specific antigen testing) unless patients are at high risk or have complications (eg, severe pneumonia, immunocompromise, asplenia, failure to respond to empiric therapy). In general, the milder the pneumonia, the less such diagnostic testing is required. Critically ill patients require the most intensive testing, as do patients in whom a antibiotic-resistant or unusual organism is suspected (eg, TB, P. jirovecii) and patients whose condition is deteriorating or who are not responding to treatment within 72 h.
Chest x-ray findings generally cannot distinguish one type of infection from another, although the following findings are suggestive:
Multilobar infiltrates suggest S. pneumoniae or Legionella pneumophila infection.
Interstitial pneumonia (on chest x-ray, appearing as increased interstial markings, subpleural reticular opacities that increase from the apex to the bases of the lungs, and peripheral honeycombing) suggests viral or mycoplasmal etiology.
Cavitating pneumonia suggests S. aureus or a fungal or mycoplasmal etiology.
Blood cultures, which are often obtained in patients hospitalized for pneumonia, can identify causative bacterial pathogens if bacteremia is present. About 12% of all patients hospitalized with pneumonia have bacteremia; S. pneumoniae accounts for two thirds of these cases.
Sputum testing can include Gram stain and culture for identification of the pathogen, but the value of these tests is uncertain because specimens often are contaminated with oral flora and overall diagnostic yield is low. Regardless, identification of a bacterial pathogen in sputum cultures allows for susceptibility testing. Obtaining sputum samples also allows for testing for viral pathogens via direct fluorescence antibody testing or PCR, but caution needs to be exercised in interpretation because 15% of healthy adults carry a respiratory virus or potential bacterial pathogen. In patients whose condition is deteriorating and in those unresponsive to broad-spectrum antibiotics, sputum should be tested with mycobacterial and fungal stains and cultures.
Sputum samples can be obtained noninvasively by simple expectoration or after hypertonic saline nebulization (induced sputum) for patients unable to produce sputum. Alternatively, patients can undergo bronchoscopy or endotracheal suctioning, either of which can be easily done through an endotracheal tube in mechanically ventilated patients. Otherwise, bronchoscopic sampling is usually done only for patients with other risk factors (eg, immunocompromise, failure of empiric therapy).
Urine testing for Legionella antigen and pneumococcal antigen is now widely available. These tests are simple and rapid and have higher sensitivity and specificity than sputum Gram stain and culture for these pathogens. Patients at risk of Legionella pneumonia (eg, severe illness, failure of outpatient antibiotic treatment, presence of pleural effusion, active alcohol abuse, recent travel) should undergo testing for urinary Legionella antigen, which remains present long after treatment is initiated, but the test detects only L. pneumophila serogroup 1 (70% of cases).
The pneumococcal antigen test is recommended for patients who are severely ill; have had unsuccessful outpatient antibiotic treatment; or who have pleural effusion, active alcohol abuse, severe liver disease, or asplenia. This test is especially useful if adequate sputum samples or blood cultures were not obtained before initiation of antibiotic therapy. A positive test can be used to tailor antibiotic therapy, though it does not provide antimicrobial susceptibility.
Short-term mortality is related to severity of illness. Mortality is < 1% in patients who are candidates for outpatient treatment. Mortality in hospitalized patients is 8%. Death may be caused by pneumonia itself, progression to sepsis syndrome (see Sepsis and Septic Shock ), or exacerbation of coexisting conditions. In patients hospitalized for pneumonia, risk of death is increased during the year after hospital discharge.
Mortality varies to some extent by pathogen. Mortality rates are highest with gram-negative bacteria and CA-MRSA. However, because these pathogens are relatively infrequent causes of pneumonia, S. pneumoniae remains the most common cause of death in patients with community-acquired pneumonia. Atypical pathogens such as Mycoplasma have a good prognosis. Mortality is higher in patients who do not respond to initial empiric antibiotics and in those whose treatment regimen does not conform with guidelines.
Risk stratification via risk prediction rules may be used to estimate mortality risk and can help guide decisions regarding hospitalization. These rules have been used to identify patients who can be safely treated as outpatients and those who require hospitalization because of high risk of complications (see Table: Risk Stratification for Community-Acquired Pneumonia (the Pneumonia Severity Index)). However, these rules should supplement, not replace, clinical judgment because many unrepresented factors, such as likelihood of adherence, ability to care for self, and wish to avoid hospitalization, should also influence triage decisions. An. ICU admission is required for patients who
Other criteria that mandate consideration of ICU admission include
The Pneumonia Severity Index (PSI) is the most studied and validated prediction rule. However, because the PSI is complex and requires several laboratory assessments, simpler rules such as CURB-65 are usually recommended for clinical use. Use of these prediction rules has led to a reduction in unnecessary hospitalizations for patients who have milder illness.
In CURB-65, 1 point is allotted for each of the following risk factors:
Scores can be used as follows:
Risk Stratification for Community-Acquired Pneumonia (the Pneumonia Severity Index)
Antibiotic therapy is the mainstay of treatment for community-acquired pneumonia. Appropriate treatment involves starting empiric antibiotics as soon as possible, preferably ≤8 h after presentation. Because organisms are difficult to identify, the empiric antibiotic regimen is selected based on likely pathogens and severity of illness. Consensus guidelines have been developed by many professional organizations; one widely used set is detailed in Community-Acquired Pneumonia in Adults (see also Infectious Diseases Society of America Clinical Guideline on Community-Acquired Pneumonia ). Guidelines should be adapted to local susceptibility patterns, drug formularies, and individual patient circumstances. If a pathogen is subsequently identified, the results of antibiotic susceptibility testing can help guide any changes in antibiotic therapy.
For children, treatment depends on age, previous vaccinations, and whether treatment is outpatient or inpatient. For outpatient treatment, treatments are dictated by age:
< 5 yr: Amoxicillin or amoxicillin/clavulanate is usually the drug of choice. If epidemiology suggests an atypical pathogen as the cause and clinical findings are compatible, a macrolide (eg, azithromycin or clarithromycin) can be used instead. Some experts suggest not using antibiotics if clinical features strongly suggest viral pneumonia.
≥ 5 yr: Amoxicillin or (particularly if an atypical pathogen cannot be excluded) amoxicillin plus a macrolide. Amoxicillin/clavulanate is an alternative. If the cause appears to be an atypical pathogen, a macrolide alone can be used.
For children treated as inpatients, antibiotic therapy tends to be more broad-spectrum and depends on the child's previous vaccinations:
Fully immunized (against S. pneumoniae and H. influenzae type b): Ampicillin or penicillin G (alternatives are ceftriaxone or cefotaxime). If MRSA is suspected, vancomycin or clindamycin is added. If an atypical pathogen cannot be excluded, a macrolide is added.
Not fully immunized: Ceftriaxone or cefotaxime (alternative is levofloxacin). If MRSA is suspected, vancomycin or clindamycin is added. If an atypical pathogen cannot be excluded, a macrolide is added.
Full details are described in the Clinical Practice Guidelines by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America .
With empiric treatment, 90% of patients with bacterial pneumonia improve. Improvement is manifested by decreased cough and dyspnea, defervescence, relief of chest pain, and decline in WBC count. Failure to improve should trigger suspicion of
An unusual organism
Resistance to the antimicrobial used for treatment
Coinfection or superinfection with a 2nd infectious agent
An obstructive endobronchial lesion
Metastatic focus of infection with reseeding (in the case of pneumococcal infection)
Nonadherence to treatment (in the case of outpatients)
If none of these conditions can be proved, treatment failure is likely due to inadequate host defenses. When therapy has failed, consultation with a pulmonary and/or infectious disease specialist is indicated.
Antiviral therapy may be indicated for select viral pneumonias. Ribavirin is not used routinely for RSV pneumonia in children or adults, but may be used in occasional high-risk children age < 24 mo.
Oseltamivir 75 mg po bid or zanamivir 10 mg inhaled bid started within 48 h of symptom onset and given for 5 days reduces the duration and severity of symptoms in patients who develop influenza infection. In patients hospitalized with confirmed influenza infection, observational studies suggest benefit even 48 h after symptom onset.
Acyclovir 5 to 10 mg/kg IV q 8 h for adults or 250 to 500 mg/m2 body surface area IV q 8 h for children is recommended for varicella lung infections. Though pure viral pneumonia does occur, superimposed bacterial infections are common and require antibiotics directed against S. pneumoniae, H. influenzae, and S. aureus.
Follow-up x-rays should be obtained 6 wk after treatment in patients > 35; persistence of an infiltrate at ≥ 6 wk raises suspicions of TB or an underlying, possibly malignant endobronchial lesion.
Community-Acquired Pneumonia in Adults
Some forms of community-acquired pneumonia are preventable with vaccination. Pneumococcal conjugate vaccine (PCV13) is recommended for children age 2 mo to 2 yr and for adults ≥ 19 yr with certain comorbid (including immunocompromising) conditions. Pneumococcal polysaccharide vaccine (PPSV23) is given to all adults ≥ 65 yr and to any patient ≥ 2 yr who has risk factors for pneumococcal infections, including but not limited to those with underlying heart, lung, or immune system disorders and those who smoke (see Table: Vaccine Administration Guidelines for Adults). The full list of indications for both pneumococcal vaccines can be seen at the CDC website. H. influenzae type b (Hib) vaccine (for patients < 2 yr), varicella vaccine (for patients < 18 mo and a later booster vaccine), and influenza vaccine (for patients age ≥ 65 and those at high risk—see Overview of Immunization and see Table: Recommended Immunization Schedule for Ages 0–6 yr) are also indicated.
In high-risk patients who are not vaccinated against influenza and household contacts of patients with influenza, oseltamivir 75 mg po once/day or zanamivir 10 po mg once/day can be given for 2 wk and started within 48 h of exposure may prevent influenza (although resistance has recently been described for oseltamivir).
Smoking cessation can reduce the risk of developing pneumonia.
Community-acquired pneumonia is a leading cause of death in the US and around the world.
Common symptoms and signs include cough, fever, chills, fatigue, dyspnea, rigors, sputum production, and pleuritic chest pain.
Treat patients with mild or moderate risk pneumonia with empiric antibiotics without testing designed to identify the underlying pathogen.
Hospitalize patients with multiple risk factors, as delineated by the risk assessment tools.
Consider alternate diagnoses, including pulmonary embolism, particularly if pneumonia-like signs and symptoms are not typical.
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