Community-Acquired Pneumonia 

Community-acquired pneumonia (CAP) is one of the most common infectious diseases addressed by clinicians. CAP is an important cause of mortality and morbidity worldwide.

A number of pathogens can give rise to CAP. Typical bacterial pathogens that cause the condition include Streptococcus pneumoniae (penicillin-sensitive and -resistant strains), Haemophilus influenzae (ampicillin-sensitive and -resistant strains), and Moraxella catarrhalis (all strains penicillin-resistant). These 3 pathogens account for approximately 85% of CAP cases.^[1]

CAP is usually acquired via inhalation or aspiration of pulmonary pathogenic organisms into a lung segment or lobe.

Less commonly, CAP results from secondary bacteremia from a distant source, such as Escherichia coli urinary tract infection and/or bacteremia.

Aspiration pneumonia is the only form of CAP caused by multiple pathogens (eg, aerobic/anaerobic oral organisms).

Severe CAP

Severe CAP develops in patients with cardiopulmonary disease, diminished splenic function, and/or pathogenic virulence. Even in young and/or healthy hosts, however, severe CAP can develop if the causative pathogen is sufficiently virulent. For example, influenza, severe acute respiratory syndrome (SARS), Hantavirus pulmonary syndrome (HPS), and Legionnaires disease may present as severe CAP.^{[2, 3, 4, 5]}

Patients with severe CAP should have the benefit of an infectious disease specialist to assist in the underlying cause of their condition.

CAP-associated complications

Complications in CAP depend on the infecting pathogen and patient health. For example, empyema can occur with Streptococcus pneumoniae, Klebsiella pneumoniae, and group A streptococcal CAP. (K pneumoniae infections occur in patients with chronic alcoholism.) Cavitation is not a feature of pneumococcal pneumonia, but it is a normal part of the disease process in K pneumoniae infections.

Myocardial infarction can be precipitated by fever due to community-acquired pneumonia (CAP).

Patients with CAP who have impaired splenic function may develop overwhelming pneumococcal sepsis, potentially leading to death within 12-24 hours, regardless of the antimicrobial regimen used.

Morbidity and mortality

CAP morbidity and mortality are highest in elderly patients and in immunocompromised hosts.

Other factors that predict an increased risk of mortality in patients with CAP include the presence of significant comorbidities, an increased respiratory rate, hypotension, fever, multilobar involvement, anemia, and hypoxia.^[6]

For more information, see the following:

• Mycoplasma Pneumonia
• Bacterial Pneumonia
• Viral Pneumonia
• Imaging Pneumocystis Carinii Pneumonia
• Aspiration Pneumonia
• Nosocomial Pneumonia
• Ventilator-Associated Pneumonia
• Pneumocystis (carinii) jiroveci Pneumonia
• Fungal Pneumonia
• Immunocompromised Pneumonia
• Nursing Home Acquired Pneumonia
• Chlamydial Pneumonia
• Lymphocytic Interstitial Pneumonia
• Imaging Typical Bacterial Pneumonia
• Imaging Atypical Bacterial Pneumonia
• Imaging Viral Pneumonia

Typical CAP pathogens

As previously mentioned, typical bacterial pathogens that cause community-acquired pneumonia (CAP) include S pneumoniae (penicillin-sensitive and -resistant strains), H influenzae (ampicillin-sensitive and -resistant strains), and M catarrhalis (all strains penicillin-resistant). These 3 pathogens account for approximately 85% of CAP cases. Gram stains of S pneumoniae, H influenzae, and M catarrhalis are seen below.

S pneumoniae remains the most common agent responsible for CAP. In patients with an exacerbation of chronic bronchitis (AECB) who develop CAP that requires hospitalization, M catarrhalis infection is the most common infecting pathogen.

Importantly, Staphylococcus aureus, K pneumoniae, and Pseudomonas aeruginosa are not typical causes of CAP in otherwise healthy hosts. S aureus may cause CAP in individuals with influenza (eg, human seasonal influenza and H1N1 [swine] influenza).^[7] K pneumoniae CAP occurs primarily in individuals with chronic alcoholism. P aeruginosa is a cause of CAP in patients with bronchiectasis or cystic fibrosis.

In certain patients admitted to the ICU, the microbial etiology of the pneumonia may be complex. In a study by Cilloniz et al, polymicrobial infection was present in 11% of cases. The most frequently identified pathogens in polymicrobial infections were S pneumoniae, respiratory viruses, and P aeruginosa. Chronic respiratory disease and acute respiratory distress syndrome criteria were independent predictors of a polymicrobic infection.^[8]

Other gram-negative pathogens (eg, Enterobacter species, Serratia species, Stenotrophomonas maltophilia, Burkholderia cepacia) rarely cause CAP.

Excluding aspiration CAP, which can be caused by multiple pathogens, virtually all cases of CAP are due to a single pathogen. Studies that report multiple pathogens in CAP are flawed and demonstrate 1 organism microbiologically, with serologic evidence of prior exposure to the other pathogen.

Atypical CAP pathogens

Atypical pneumonias can be divided into those caused by either zoonotic or nonzoonotic atypical pathogens.

Zoonotic atypical CAP pathogens include Chlamydophila (Chlamydia) psittaci (psittacosis), Francisella tularensis (tularemia), and Coxiella burnetii (Q fever).

Nonzoonotic atypical CAP pathogens include Legionella species, M pneumoniae, and Chlamydophila (Chlamydia) pneumoniae.^[9] These organisms account for approximately 15% of all CAP cases.

The clinical diagnosis of typical and atypical CAP is diagrammed below.

Prevalence in the United States

The number of annual community-acquired pneumonia (CAP) cases is difficult to estimate. One study, in which 46,237 elderly patients were monitored over a 3-year period, showed the rate of CAP among those aged 65-69 years to be 18.2 cases per 1000 person-years. Among person older than age 85 years, the rate was 52.3 cases per 1000 person-years. Estimates based on this data suggested that annually, 1 of 20 persons older than 85 years develop CAP. The investigators also estimated that approximately 915,900 cases of CAP occur among the elderly population annually in the United States.^{[10, 11, 12]}

International prevalence

The distribution and prevalence of zoonotic CAPs is higher internationally than in the United States because of the density and distribution of zoonotic vectors.

Age in CAP

Patients who require hospital treatment for CAP are typically elderly persons; persons with underlying chronic obstructive pulmonary disease (COPD), such as chronic bronchitis (not emphysema); and individuals with severe CAP related to underlying cardiopulmonary function, immune status, or pathogen virulence.^[13]

Ambulatory CAP is most common among young adults and is usually due to atypical CAP pathogens (eg, Mycoplasma pneumoniae).^[14]

Negative prognostic factors in community-acquired pneumonia (CAP) include preexisting lung disease, underlying cardiac disease, poor splenic function, advanced age, multilobar involvement, and delayed initiation of appropriate antimicrobial therapy. Obviously, when all other factors are equal, older patients do not fare as well as younger adults.^[15]

Bacteremia is part of the disease process in pneumococcal pneumonia and is not a complication or a bad prognostic sign in this disorder.

Typical bacterial community-acquired pneumonias (CAPs) have no extrapulmonary findings. In contrast, each atypical pathogen has its own distinctive pattern of extrapulmonary organ involvement, which is the basis for a presumptive clinical diagnosis. Extrapulmonary characteristics of atypical CAP are outlined in Table 1.

Table 1. Differential Diagnostic Features of Atypical Pneumonias^[16] (Open Table in a new window)

Although Q fever and psittacosis are associated with relative bradycardia, these zoonotic pneumonias may be excluded by a negative recent or close vector contact history.

Relative bradycardia in a patient with CAP should suggest Legionnaires disease if psittacosis and Q fever are eliminated from the diagnostic consideration by zoonotic contact history. The characteristics and causes of relative bradycardia are outlined in Table 2.

Table 2. Relative Bradycardia (Open Table in a new window)

Because Legionella pneumonia has its own characteristic pattern of organ involvement (demonstrated in the images below), it is readily distinguished from other typical and atypical pathogens.

Some signs and symptoms are more important than others and can be expressed in a weighted diagnostic point system, which is accurate in making a presumptive clinical diagnosis of Legionnaires disease. (See Table 3 below.)

Table 3. Modified Winthrop University Hospital Infectious Disease Division's Point System for Diagnosing Legionnaires Disease in Adults^[16] (Open Table in a new window)

CAP and shock

In otherwise healthy hosts, CAP does not present with shock. CAP that presents with shock in the absence of conditions associated with hyposplenism should prompt an evaluation for mimics of pneumonia that manifest as pulmonary infiltrates on chest radiography, fever, leukocytosis, and hypotension, such as acute myocardial infarction or acute pulmonary embolism.

If CAP manifests as shock without evidence of hyposplenia, acute myocardial infarction, or acute pulmonary embolism, consider an exacerbation of preexisting cardiopulmonary disease that presents with hypotension and coronary insufficiency with hypoxemia or emphysema

If CAP presents with shock and cardiac/pulmonary causes have been excluded, look for impaired or absent splenic function. Disorders and therapies associated with impaired splenic function include the following:

• Chronic alcoholism
• Amyloidosis
• Chronic active hepatitis
• Fanconi syndrome
• Hyposplenism in elderly patients
• Immunoglobulin A (IgA) deficiency
• Intestinal lymphangiectasia
• Myeloproliferative disorders
• Waldenström macroglobulinemia
• Non-Hodgkin lymphoma
• Celiac disease
• Regional enteritis
• Sézary syndrome
• Congenital asplenia
• Splenectomy
• Sickle cell trait/disease
• Splenic infarcts
• Splenic malignancies
• Steroid therapy
• Rheumatoid arthritis
• Systemic lupus erythematosus (SLE)
• Systemic mastocytosis
• Systemic necrotizing vasculitis
• Thyroiditis
• Pulmonary embolism
• Congestive heart failure or acute myocardial infarction

Patients with community-acquired pneumonia (CAP) due to typical bacterial CAP pathogens present with pulmonary symptoms, while patients with CAP due to atypical CAP pathogens present with a variety of pulmonary and extrapulmonary findings (eg, CAP plus diarrhea).

Patients with bacterial CAP typically present with fever, usually with a productive cough and often with pleuritic chest pain.

The clinical presentation of atypical CAP is often subacute. CAP due to atypical pathogens has 1 or more extrapulmonary features, which is a clue to the etiology.

Patients with Legionella pneumonia may have a productive or nonproductive cough. In contrast, patients with pneumonia due to M pneumoniae or Chlamydophila (formerly Chlamydia) pneumoniae usually present with a nonproductive cough.

With the exception of Legionella pneumonia, pleuritic chest pain is typically not a feature of CAP due to nonzoonotic atypical pathogens.

Zoonotic infection

Recent and/or close contact with the appropriate zoonotic vector is needed to develop a zoonotic CAP. A history of close contact with a parturient cat or sheep should be sought in patients with suspected Q fever. Psittacosis is preceded by recent and/or close contact with psittacine birds. Patients with tularemia have had recent close contact with deer or rabbits or have recently been bitten by a tick or deer fly.

Physical findings are confined to the lungs in patients with typical bacterial community-acquired pneumonia (CAP).

Purulent sputum is characteristic of pneumonia caused by typical bacterial CAP pathogens and is not usually a feature of that caused by atypical pathogens, with the exception of Legionnaires disease. Blood-tinged sputum may be found in patients with pneumococcal pneumonia, Klebsiella pneumonia, or Legionella pneumonia.

Rales are heard over the involved lobe or segment. If consolidation is present, an increase in tactile fremitus, bronchial breathing, and E to A change may be present.

Legionella pneumonia, Q fever, and psittacosis are atypical pneumonias that may present with signs of consolidation. Consolidation is not a feature of pneumonia caused by M pneumoniae or Chlamydophila (Chlamydia) pneumoniae.^[9]

Be wary when a patient presents with severe CAP, with or without hypotension or shock. In these patients, be sure to exclude an underlying acute pulmonary or cardiac event that could explain the severity of the CAP.

In addition, if the severity of CAP or hypotension is not apparently due to cardiopulmonary factors, consider unrelated conditions that may present in a similar clinical fashion, such as acute gastrointestinal bleeding, pancreatitis, or adrenal insufficiency.

Pleural effusion

Pleural effusion (usually due to H influenzae infection), if large enough, is detectable on physical examination. Patients with pleural effusion have decreased tactile fremitus and dullness on chest percussion.

Pleural effusion in a patient with CAP and extrapulmonary manifestations should suggest Legionella infection. Pleural effusion with appropriate epidemiologic history findings, such as contact with a rabbit or deer, may suggest tularemia. CAP with a large pleural effusion (serosanguineous) is typical of that caused by group A streptococci.

Empyema

On physical examination, empyema has the same findings as pleural effusion. Empyema is most often associated with Klebsiella, group A streptococci, and S pneumoniae.

Aside from those mentioned above (see Extrapulmonary Findings in Atypical CAP), differentials to consider in the diagnosis of community-acquired pneumonia (CAP) include the following:

• Acute bronchitis
• AECB
• Myocardial infarction
• Congestive heart failure and pulmonary edema
• Pulmonary fibrosis
• Sarcoidosis
• SLE pneumonitis
• Pulmonary drug hypersensitivity reactions (nitrofurantoin)
• Drug-induced pulmonary disease
• Pulmonary embolus or infarction
• Bronchogenic carcinomas
• Radiation pneumonitis
• Wegener granulomatosis
• Lymphomas
• Tracheobronchitis

Send the sputum of patients with community-acquired pneumonia (CAP) for Gram stain and/or culture. Keep in mind that many patients, especially elderly persons, are not able to produce an adequate suitable sputum sample.

Sputum Gram stain is reliable and diagnostic if performed on a well-collected specimen without many squamous epithelial cells (saliva/contamination) and a predominant organism is present. Gram stain shows few or no predominant organisms in patients with atypical CAPS.

Do not send the sputum of patients with COPD (eg, AECB) for Gram stain or culture, because these patients invariably demonstrate a mixed or normal flora.

Obtain blood cultures from all patients with CAP upon admission, because some typical bacterial pathogens, such as S pneumoniae and H influenzae, are frequently associated with positive blood cultures. M catarrhalis bacteremia is rare.

The differential diagnosis of the pathogen responsible for community-acquired pneumonia (CAP) in patients with the human immunodeficiency virus (HIV) is determined by assessing the CD4 count and the chest radiographic appearance.

Patients with HIV infection and a normal or slightly decreased CD4 count with focal infiltrates have approximately the same pathogen distribution as otherwise healthy hosts (eg, S pneumoniae). Patients with nonfocal infiltrates and hypoxemia may have Pneumocystis (carinii) jiroveci pneumonia (PCP). Patients with HIV infection and focal infiltrates may have tuberculosis, which is easily diagnosed using acid-fast bacillus (AFB) smears of sputum.

In patients with HIV infection in whom S pneumoniae CAP is suspected, urinary antigen testing may be useful.

These are typically performed if, based on extrapulmonary findings, atypical community-acquired pneumonia (CAP) is suspected.

Workup should include serum transaminase levels, serum phosphorous levels, urinalysis, ferritin levels, creatine phosphokinase (CPK) levels, C-reactive protein (CRP) levels, and cold agglutinin titers.

Otherwise unexplained early, transient, and slight increases in serum transaminases in a patient with CAP suggest the presence of psittacosis, Q fever, or Legionella pneumonia.^[17]

Otherwise unexplained hypophosphatemia or microscopic hematuria in a patient with CAP suggests Legionnaires disease.^[18]

Agglutinin levels

Low-titer cold agglutinin elevations occur in various viral and neoplastic illnesses. Of patients with Mycoplasma pneumonia, 75% develop transient elevations of cold agglutinins 1-2 weeks into the illness.

A negative cold agglutinin titer finding does not exclude Mycoplasma species.

A moderately elevated cold agglutinin titer effectively rules out Legionella pneumonia. Because low titer elevations of cold agglutinins are nonspecific, the diagnosis of Mycoplasma pneumonia is likely only if the cold agglutinin titer is highly elevated (>1:64) in a patient with CAP.

Direct fluorescent antibody testing

In a patient with suspected Legionella pneumonia, direct fluorescent antibody (DFA) testing of the sputum can assist in diagnosis if obtained early and before antimicrobial treatment. Antimicrobial treatment rapidly decreases the sputum yield of DFA testing. A DFA stain showing Legionella infection is seen in the image below.

Serology for zoonotic pathogens

Send serology if zoonotic atypical pathogens are suspected, because isolation and culture are difficult and dangerous for microbiology personnel. Diagnosis of zoonotic pathogen–associated pneumonia is based on a 4-fold or greater increase in titers between acute- and convalescent-phase serum specimens.

Immunoglobulin studies

Obtain immunoglobulin M (IgM) and immunoglobulin G (IgG) titers for C pneumoniae and M pneumoniae if they are a diagnostic possibility. An increase in the IgG titer for either organism suggests past exposure and does not indicate acute infection. An increase in the IgM titer for either pathogen allows the diagnosis in a patient with CAP.

If Chlamydophila (Chlamydia) pneumoniae infection is suspected, obtain specific pneumonia IgM and IgG titers. Do not obtain chlamydial titers without specifying the species.^[9]

Legionella serology

Obtain Legionella serologies if Legionella pneumonia is suggested based on the pattern of extrapulmonary findings. However, negative acute titer findings do not rule out Legionnaires disease, because titers may not rise for 6-8 weeks. The finding of an initially high Legionella titer is unusual, and clinical diagnosis rests on demonstrating a 4-fold or greater increase between acute- and convalescent-phase titers.

Peripheral smear

Impaired splenic function is determined by demonstrating Howell-Jolly bodies or "pitted red blood cells" in the peripheral smear. The number of Howell-Jolly bodies is inversely proportional to splenic function.

Urinary antigen test

In patients with CAP who produce no sputum, a positive urinary antigen test for S pneumoniae, if suspected, confirms the diagnosis of pneumococcal CAP.^[19]

The Legionella urinary antigen test is applicable only for the Legionella pneumophila serogroup type I, which accounts for approximately 80% of infections. The urinary antigen test remains positive for Legionella for long periods but may be negative early in the infection.

Chest radiography

Obtain chest radiographs in all patients with suspected community-acquired pneumonia (CAP) to exclude conditions that mimic CAP and to confirm the presence of an infiltrate compatible with the presentation of CAP.^{[20, 21]} (See the images below.)

Patients presenting very early with CAP may have negative findings on chest radiography. In these patients, repeat chest radiography within 24 hours.

Chest radiography assists with the differentiation of viral pneumonias from nonviral pneumonias. Viral pneumonias display few or no infiltrates on chest radiography, but when infiltrates are present, they are almost always bilateral, perihilar, symmetric, and interstitial.

Bacterial pneumonias have a predominantly focal segmental or lobar distribution. In contrast, typical or atypical pathogens produce a lobar or segmental pattern on chest radiography, with or without consolidation or pleural effusion.

Chest radiographic findings should be negative in patients with asthma who do not have CAP. Chest radiographs are also negative in patients with AECB.

The infiltrates observed with congestive heart failure (CHF) appear as increased interstitial markings and show vascular redistribution to the upper lobes. Patients with preexisting heart failure usually have cardiomegaly.

Rapid cavitation is not a typical feature of CAP.

Community-acquired, methicillin-resistant S aureus (CA-MRSA) CAP presents as a fulminant CAP with rapid cavitation and necrotizing pneumonia caused by CA-MRSA (SCC mec IV) with the PVL gene, which occurs with influenza.

Aspiration pneumonitis may develop cavitation 1 week after aspiration. Signs of cavitation are absent on the initial chest radiograph in patients with CAP due to aspiration.

Serial chest radiography can be used to observe the progression of CAP. Rapidly progressive, asymmetric infiltrates suggest the possibility of Legionnaires disease. Chest radiographic findings worsen rapidly and require a significant period to improve. Clinical resolution occurs long before radiologic resolution.

CT scanning

Obtain a computed tomography (CT) scan of the chest when an underlying bronchogenic carcinoma is suggested or if any abnormalities are not consistent with the diagnosis of pneumonia only.

Transthoracic fine-needle aspiration (FNA) of the infiltrate can be performed and is most useful in determining the cause of noninfectious-associated infiltrates that are not responding to antibiotic treatment.

Transtracheal aspiration (TTA) is a potentially hazardous procedure and offers no additional diagnostic information in patients with community-acquired pneumonia (CAP).

Diagnostic bronchoscopy with bronchoalveolar lavage (BAL) may be useful in patients with CAP when PCP is a likely diagnostic possibility. Diagnostic bronchi with BAL may also be useful in unresolving CAP that does not respond to appropriate therapy.

Lung sections with typical bacterial pneumonias show the progression from red hepatization to white hepatization during the resolution process. The lung is repaired after bacterial pneumonia is complete and the infectious process resolves.

Although patients with mild community-acquired pneumonia (CAP) may be treated in an ambulatory setting, patients with CAP who are moderately to severely ill should be hospitalized. This is true for children as well, according to the first-ever guidelines for the management of infants and children with CAP released by The Infectious Diseases Society of America (ISDA) in 2011.^[22] Patients with severe CAP, including children who require invasive ventilation via a nonpermanent artificial airway, require admission to an intensive care unit (ICU). Oxygen and/or ventilatory support may be required.^{[4, 23, 24, 25, 26, 27]}

Because the severity of CAP frequently is due to underlying severe cardiopulmonary disease, direct medical efforts at supporting cardiopulmonary function while administering antibiotics for CAP.

Patients admitted with severe CAP and hypotension or shock are often hypotensive because of an acute pulmonary or cardiac insult, such as pulmonary embolism or acute myocardial infarction.

If no acute cardiopulmonary explanation can be found (eg, exacerbation of severe underlying lung disease, exacerbation of preexisting CHF), patients with shock likely have diminished or absent splenic function.

Patients with CAP who have severe cardiopulmonary disease or hyposplenic dysfunction have a prolonged course that may require transfer to a subacute unit with less-intensive care.

There is no optimal therapy for community-acquired pneumonia (CAP). Most experts feel that coverage should be divided against typical and atypical CAP pathogens.^[28]

CAP may be treated with monotherapy or combination therapy. Effective monotherapy antibiotics include doxycycline, respiratory quinolones, or tigecycline.^{[29, 30, 31, 13]}

Combination therapy usually consists of ceftriaxone plus doxycycline, azithromycin, or a respiratory quinolone. Alternately, some physicians use a quinolone-based approach. Quinolones vary by country and are updated periodically. Immunocompromised hosts who present with CAP are treated in the same manner as otherwise healthy hosts but may require a longer duration of therapy.

Most patients with CAP who are admitted to the hospital are treated with intravenous medications initially and then complete a 12-day oral course of therapy for a total of 14 days of combined intravenous and oral therapy.^{[32, 33, 34, 35]}

Patients who are severely ill or who are unable to tolerate or absorb oral medications require a longer duration of intravenous therapy before switching to an oral antibiotic.^[36]

Mild to moderately ill patients with CAP may be treated entirely via the oral route, either on an inpatient or outpatient basis. Patients receiving oral antibiotics may be admitted for hospital services (eg, pulmonary toilet and additional diagnostic tests) that are not obtainable on an outpatient basis.

If the patient is switched to an oral regimen and is doing well, earlier discharge from the hospital is possible. The oral therapy regimen can be completed at home. Optimal intravenous-to-oral switch therapy consists of a single agent that has an appropriate spectrum, has excellent bioavailability, is well tolerated, has a low resistance potential, and is relatively inexpensive.

Very healthy young adults and children may be treated for shorter periods.

Comorbid conditions

Comorbid conditions do not affect the selection of antimicrobial therapy. The addition and/or change of antibiotics based on the severity of illness and/or comorbidities makes little sense. Antimicrobial therapy is directed against the pathogen rather than against the comorbid factors. Comorbidity is an important prognostic factor and contributes to the severity index but has no place in antibiotic selection.^[15]

Severity

The severity of CAP is determined by underlying conditions of the lungs, heart, and spleen. Do not change antibiotics or use additional antibiotics to treat severe CAP. Additional antibiotics do not affect the pulmonary, cardiac, or splenic dysfunction that determines clinical severity.

In aspiration pneumonia, the extent of aspiration and lobar distribution of the infiltrates depends on the patient's position at the time of aspiration.

Appropriate spectrum

In otherwise healthy hosts, therapy does not need to cover S aureus, Klebsiella species, or P aeruginosa in CAP. (Most CAP regimens include K pneumoniae coverage.) S aureus coverage should be included in patients with influenza who have focal infiltrates.

Most antibiotics used to treat community-acquired aspiration pneumonia (eg, doxycycline, respiratory quinolones, beta lactams) are highly effective against oral anaerobes. Metronidazole and clindamycin are unnecessary. For aerobic lung abscesses, clindamycin or moxifloxacin is preferable.^{[37, 38, 39, 40]} Coverage should include the typical (S pneumoniae, H influenzae, M catarrhalis) and atypical (Legionella and Mycoplasma species, C pneumoniae) pathogens.

Monotherapy

Monotherapy coverage of typical and atypical pathogens in CAP is preferred over double-drug therapy; monotherapy is less expensive than double-drug regimens are, while being just as effective.^[30]

Avoid empiric macrolide monotherapy, because approximately 25% of S pneumoniae strains are naturally resistant to all macrolides.^{[41, 42, 43]}

Preferred monotherapy for CAP includes doxycycline or a respiratory quinolone. This is the most cost-effective way to optimally treat CAP. No increased resistance is noted with extensive use. It is well tolerated in oral and intravenous forms. It is ideal for intravenous-to-oral switch monotherapy in terms of patient compliance, safety, and cost.^{[44, 45]}

Penicillin resistance

Most penicillin resistance is "relative resistance" and is readily treatable with penicillin and/or beta lactams.^[43]

Most highly penicillin-resistant S pneumoniae infections may also be treated with beta lactams. Alternately, doxycycline or respiratory quinolones may be used. Vancomycin is rarely, if ever, needed.

Very highly penicillin-resistant S pneumoniae (MIC 6 µg/mL) strains are a rare cause of CAP; they remain susceptible to ceftriaxone.

PPIs

Avoid using proton-pump inhibitors (PPIs) when using respiratory quinolones for CAP drug therapy. Either stop the PPI or use a histamine-2 (H2) blocker for the duration of therapy. However, there is conflicting evidence as to the safety of using PPIs and H2 blockers.^{[46, 47, 48, 49]}

In a study, Eurich et al concluded that the use of acid suppressants substantially increases the risk of recurrent pneumonia in high-risk elderly patients. In a cohort of elderly patients who had previously been hospitalized for pneumonia, the investigators classified PPI and H2 use during 5.4 years of follow-up, matching 248 patients with recurrent pneumonia with 2476 controls.^[46]

Patients in the study who were currently using PPI/H2 had a higher rate of recurrent pneumonia than did nonusers (12% vs 8%, respectively).

In contrast, a population-based, nested case-control study by Dublin et al concluded that PPIs and H2 blockers do not increase the risk of pneumonia in older adults.^[48]

Monitor patients with mild community-acquired pneumonia (CAP) who are being treated on an outpatient basis to be sure that they are compliant with their medications and that they are improving. After 1 week, a repeat visit and chest radiography is advisable. As long as the patient is improving and parapneumonic complications are not evident, posttherapy chest radiography is unnecessary.^{[50, 51, 52]}

Diet in patients with CAP is as tolerated. Guide activity with common sense.

Pneumococcal vaccines prevent pneumococcal bacteremia but not necessarily pneumococcal pneumonia.^[53] Two pneumococcal vaccines are approved in the United States. Prevnar 13, a pneumococcal 13-valent conjugate vaccine is approved for children aged 6 weeks to 5 years and adults aged 50 years or older. The 23-valent vaccine (Pneumovax 23) is approved for adults aged 50 years or older and persons aged 2 years or older who are at increased risk for penumococcal disease.

Nonleukopenic compromised hosts, such as those with rheumatoid arthritis, SLE, or alcoholism, may not develop an antibody response to the pneumococcal vaccine and may therefore remain susceptible to pneumococcal pneumonia. The same is true concerning the use of the Haemophilus vaccine.

Remind patients with community-acquired pneumonia (CAP) to comply with the medication even after they experience clinical improvement. Except in patients with heart failure, adequate hydration and preservation of the cough reflex during the convalescent period are important.

For patient education information, see eMedicine's Pneumonia Center, as well as Bacterial Pneumonia.