Community-Acquired Pneumonia (CAP) Update Year 2000: Current Antibiotic Guidelines and Outcome-Effective Management: Part I
Community-Acquired Pneumonia (CAP) Update Year 2000: Current Antibiotic Guidelines and Outcome-Effective Management: Part I
Authors: Charles L. Emerman, MD, Associate Professor of Emergency Medicine, Case Western Reserve University; Chairman, Department of Emergency Medicine, MetroHealth Medical Center and The Cleveland Clinic Foundation, Cleveland OH. Gideon Bosker, MD, FACEP, Assistant Clinical Professor, Section of Emergency Services, Yale University School of Medicine; Associ- ate Clinical Professor, Oregon Health Sciences University. Lisa A. Miller, MD, Department of Emergency Medicine, MetroHealth Medical Center, Cleveland, OH.
Peer Reviewers: Jonathan Edlow, MD, Vice Chairman, Department of Emer- gency Medicine, Beth Istael Deaconess Medical Center; Assistant Professor, Harvard Medical School, Boston, MA; Stephen P. Ernst, PharmD, Clinical Pharmacy Coordinator, Columbia Terre Haute Regional Hospital, Terre Haute, IN; Sandra M. Schneider, MD, Professor and Chair, Department of Emer- gency Medicine, University of Rochester, Rochester, NY. Steven M. Winograd, MD, FACEP, Attending Physician, Department of Emergency Medicine, Sturgis Hospital, Sturgis, MI, and Allegan General Hospital, Allegan, MI.
Among common infections managed in the emergency department, ambulatory care clinic, or hospital setting, few conditions have had treatment guidelines, antibiotic selection strategies, or institutional protocols change or evolve as rapidly as they have for community-acquired pneumonia (CAP). For a number of reasons, it has become extremely difficult for clinicians to keep current with antibiotic protocols and risk-stratification criteria for CAP. Despite a general consensus that empiric treatment of CAP in adults requires, at the very least, mandatory coverage of such organisms as S. pneumoniae, H. influenzae, M. catarrhalis, as well as atypical organisms (M. pneumoniae, C. pneumoniae, and L. pneumophila), antibiotic selection strategies for achieving this spectrum of coverage vary widely.
There are many reasons for the inconsistencies in the current approach to CAP management among emergency departments, pulmonologists, and hospitals. First, over the past year, of two expanded-spectrum quinolone antibiotics which showed early promise for treatment of CAP, one agent has had its use significantly restricted, while the other has been removed from the market as a result of drug-related side effects. Second, new treatment guidelines for CAP have been issued by some national associations (Infectious Disease Society of America) and consensus panels, whereas other treatment protocols for pneumonia still in force (and are now several years old) were generated by other influential associations and need revision. Deciphering the strengths and weaknesses of recommendations issued by different authoritative sources can be problematic and confusing, to say the least. Third, because patient disposition practices and treatment pathways vary among institutions and from region to region, management guidelines for CAP must be "customized" for the local practice environment.
Unfortunately, no single set of guidelines is applicable to every patient or practice environment; therefore, clinical judgment must prevail. This means taking into account local antibiotic resistance patterns, epidemiological and infection incidence data, and patient demographic features. Even when these factors are considered, a number of important questions and drug selection issues still remain: 1) When is intravenous monotherapy for pneumonia an outcome-effective management strategy? When is two-drug therapy the appropriate course? 2) What are the specific "intensification and treatment trigger" criteria that support amplifying spectrum of coverage from a macrolide to an extended spectrum fluoroquinolone? 3) Which macrolides are available for intravenous-to-oral, step-down therapy? 4) What is the role of risk stratification guidelines for intial antibiotic selection in CAP?
It is becoming clear the outcomes for CAP can be maximized by using risk-stratification criteria that predict mortality associated with CAP. Associated clinical findings such as hypotension, tachypnea, impaired oxygen saturation, multi-lobar involvement, elevated blood urea nitrogen, and altered level of consciousness are predictive of more serious disease, just as age and acquisition of CAP in a nursing home environment are. These factors may assist clinicians in initial selection of intravenous antibiotic therapy for hospitalized patients.
Because of important advances, changes, and refinements that have occurred in the area of CAP treatment over the past year, the authors of this comprehensive, state-of-the-art review present a revised and updated set of guidelines outlining CAP management for the year 2000. Special emphasis has been given to both epidemiological data demonstrating the importance of "correct spectrum" coverage with specific macrolides or fluoroquinolones and to the selection of initial intravenous antibiotics for in-hospital management of CAP.
In addition, a detailed analysis of monotherapeutic (azithromycin or levofloxacin)) vs. two-drug (cephalosporin plus a macrolide) approaches for initial therapy is also provided. To ensure our readers are current with the latest evidence-based strategies for CAP treatment, detailed antibiotic selection guidelines—presented in the form of rapid-access treatment tables—are provided. Drawing upon consensus panels and association guidelines, these antimicrobial protocols are linked to risk-stratification criteria and specific clinical profiles in patients presenting to the hospital or ambulatory setting with CAP.
— The Editor
Introduction
CAP is a common problem and a potentially life-threatening condition that accounts for about 500,000 adult hospitalizations and 1.2 million emergency department (ED) visits annually.1 Although this infectious disease affects individuals of all ages, pneumonia is a more frequent problem in young children and in older adults. The annual incidence of pneumonia in patients older than 65 years is about 1%.1 The typical presentation of pneumococcal pneumonia with fever, rigors, shortness of breath, chest pain, sputum production, and abnormal lung sounds is easy to recognize. Unfortunately, the changing epidemiology of pneumonia presents a greater diagnostic challenge. Atypical agents or opportunistic infections in immunocompromised patients have a much more subtle presentation. And pneumonia in young children may not present with classical findings, whereas older patients frequently have an insidious presentation with fewer characteristic features of pneumonia.2
Triage. Hospitalization of patients with pneumonia is costly, although many patients with CAP can be safely managed as outpatients. In the absence of respiratory distress or other complicating factors, many children and young adults can be adequately treated with appropriate oral antibiotic therapy. Even following appropriate treatment, however, patients may have symptoms, including cough, fatigue, dyspnea, sputum production, and chest pain that last for several months.3 A variety of investigators have proposed criteria to identify patients requiring hospitalization. Patients felt to be at "low" risk have a median length of stay of seven days, while those at "medium" risk have a median length of stay of 12-13 days.4
Among the factors physicians use to make admission decisions for pneumonia are the presence of hypoxemia, the ability to maintain oral intake, and the patient’s home situation.9 Using clinical judgment, however, physicians tend to overestimate the likelihood of death from pneumonia.9 These findings have led some investigators to employ more stringent prediction rules. For example, the chest radiograph may help to identify patients at high risk for mortality.10 The presence of bilateral effusions, moderate-size pleural effusions, multi-lobar involvement, and bilateral infiltrates are associated with a higher risk of mortality. On the other hand, the presence of air bronchograms lessens the likelihood of death.11
A recent landmark study outlined a prediction rule to identify low-risk patients with CAP.12 (See Table 1.) Using patient age, coexistent medical conditions, and vital signs, patients are assigned either to a low-risk class, which has a mortality rate of about 0.1% in outpatients, or to higher risk categories. (See Figure 1.) Patients with any risk factors are then evaluated with a second scoring system that assigns individuals to one of three higher risk categories, which have mortality rates that range from 0.7% to 31%.12 In addition to the factors noted in this prediction rule, patients who are immunocompromised as a result of AIDS or chronic alcohol use frequently require hospitalization.
| Table 1. Assignment to Risk Classes II-V for Prediction of Mortality from Pneumonia | |
| Assignment of risk points | |
| Criteria | Points |
| Female gender | -10 |
| Nursing home | 10 |
| Coexistent illness | |
| Neoplastic disease | 30 |
| CHF | 20 |
| CVA | 10 |
| Renal disease | 10 |
| Liver disease | 10 |
| Abnormal exam | |
| Abnormal mental status | 20 |
| Pulse Þ 125 | 20 |
| RR Þ 30 | 20 |
| BP Ü 90 | 15 |
| Temperature < 35°C or > 40°C | 10 |
| Lab and x-ray | |
| pH < 7.35 | 30 |
| BUN Þ 30 | 20 |
| Na < 130 | 20 |
| Glucose Þ 250 | 10 |
| Hematocrit < 30% | 10 |
| PaO2 < 60 mmHg | 10 |
| Pleural effusion | 10 |
| Class stratification | |
Once the clinician has determined hospitalization is required, the need for intensive care unit admission must also be evaluated. In this regard, a variety of factors are associated with an increased risk for mortality, including increasing age, alcoholism, chronic lung disease, immunodeficiency, and specific laboratory abnormalities.13,14 The American Thoracic Society guidelines for the identification of patients at high risk for mortality is presented in Table 2.15
| Table 2. Identification of Patients at High Risk for Mortality | |
| 1. Respiratory rate > 30 per minute | |
| 2. PaO2/FIO2 ratio less than 250 | |
| 3. Ventilatory support | |
| 4. Multi-lobar, bilateral, or greater than 50% infiltrates | |
| 5. Systolic blood pressure less than 90 mmHg | |
| 6. Diastolic blood pressure less than 60 mmHg | |
| 7. Necessity for vasopressors | |
| 8. Urine output less than 20 mL/hour | |
| Source: American Thoracic Society | |
Diagnosis and Evaluation
The definitive diagnosis of pneumonia is verified by the recovery of a pathogenic organism(s) from either the blood, sputum, or pleural fluid in the setting of a patient with a radiographic abnormality suggestive of pneumonia. In the case of atypical organisms, the diagnosis is made by the comparison of acute and convalescent sera demonstrating a rise in appropriate titers, or by other sophisticated techniques such as direct florescent antibody testing. The Gram’s stain is occasionally helpful in establishing the diagnosis, but requires practitioners or technicians highly skilled in this diagnostic methodology. An adequate Gram’s stain must have fewer than 25 epithelial cells per low-powered field.16 The finding of more than 10 gram-positive, lancet shaped diplococci in a high-powered field is a sensitive and specific predictor of pneumococcal pneumonia.16 Unfortunately, the Gram’s stain will rarely be helpful in determining other causes of pneumonia.17
Transtracheal aspiration or bronchial washings are a more accurate means of obtaining specimens for Gram’s stains and culture, although this procedure is rarely indicated in the outpatient setting. Overall, fewer than 50% of patients with a CAP will be able to produce sputum.18 Of these, half of the sputum specimens obtained will be inadequate.17,19 When an adequate Gram’s stain is obtained, however, it has a negative predictive value of 80% when compared to a sputum culture.20 The blood culture is helpful in about 15% of patients, while serology will establish the diagnosis in 25% of patients.21 About 40% of sputum cultures will identify a pathologic organism. Bronchoscopy and thoracentesis may occasionally be necessary, but these procedures generally are reserved for seriously ill patients, particularly those who require management in the intensive care unit setting.
The signs and symptoms of pneumonia may be mimicked by many disorders, including pulmonary embolism, lung cancer, hypersensitivity pneumonitis, tuberculosis, chronic obstructive pulmonary disease (COPD), granulomatosis disease, and fungal infections.22 A variety of drugs also can induce pulmonary disease. Cytotoxic agents, non-steroidal anti-inflammatory drugs (NSAIDs), and some antibiotics, including sulfononamides, as well as certain antiarrhythmics such as amiodarone or tocainide, can mimic pulmonary infection. In addition, common analgesics, including salicylates, propoxyphene, and methadone may also precipitate acute respiratory symptoms. Such collagen vascular diseases as systemic lupus erythematosus, polymyositis, and polyarteritis nodosa may cause fever, cough, dyspnea, and pulmonary infiltrates, thereby mimicking symptoms of pneumonia. Rheumatoid arthritis can cause an interstitial lung disease, although it does not usually cause fever or alveolar infiltrates.23
Radiographic Features
Although atypical etiologies of pneumonia (Mycoplasma, Chlamydia, Legionella) tend to have a different radiographic presentation than that seen in patients with bacterial pneumonia, clinical distinctions based on radiographic features are difficult, if not impossible, in the majority of cases. Patients with bacterial pneumonia are more likely to have unilobar pneumonia as compared to patients infected with atypical agents.24 Lobar or segmental collapse is most common in patients with atypical pneumonia, as is hilar adenopathy. In general, patients with bacterial pneumonia are more likely to have cavitary lesions, effusion, and bulging of the fissures compared to patients with an atypical cause of their pneumonia. In addition, patients with atypical pneumonia are more likely to have nodular or reticular infiltrates, and perihilar adenopathy.25 (See Table 3.)
| Table 3. Signs and Symptoms of Community-Acquired Pneumonia | ||||
| Organism | Population at risk | Typical symptoms | Other findings | Radiographic appearance |
| S. pneumoniae | all, but children and elderly at greater risk | sudden onset, fever, chills, pleuritic chest pain | herpes simplex | lobar pneumonia pleural effusions, "round" infiltrates |
| H. influenzae | older patients, COPD, alcoholics | gradual onset bronchitis, dyspnea chest pain | rales consolidative or patchy lobular pattern | |
| S. aureus | nursing home patients post-influenza infection | gradual onset fever, sputum, dyspnea | hemoptysis | multi-lobar infiltrate effusion, empyema, abscess |
| K. pneumoniae | alcoholics, nursing home patients | sudden onset, chest pain, dyspnea, bloody sputum | toxic appearance | multi-lobular infiltrate effusion, empyema, abcess |
| B. catarrhalis | COPD, incidence increases during winter months | gradual onset, cough, fever retrosternal chest pain, wheezing | petechial rashes | interstitial pattern |
| L. pneumophila | COPD, smokers | gradual onset, pleuritic chest, pain, GI disturbance, shaking chills | hyponatremia, altered mental status, sinusitis | patchy localized infiltrate |
| M. pneumoniae | children, young adults | gradual onset, malaise, fever, headache | pharyngitis, adenopathy, cunjunctivitis, sinusitis | patchy localized infiltrate |
| Chlamydia TWAR | all, but incidence increases with age | gradual onset, cough, fever, wheezing | sinusitis | subsegmental infiltrates |
| Anaerobic organisms | alcoholics | gradual onset, putrid sputum | weight loss | upper segments of lower lobes, lower segments of upper lobes |
| Q fever | exposure to livestock or parturient cats | sudden onset, high fever, chills | severe headache, hepatomegaly | rounded densities |
| Tularemia | exposure to ticks, rabbits, squirrels | pleuritic chest pain | rashes | variable, may have ovoid infiltrates |
| Psittacosis | exposure to birds | sudden onset, chest pain | severe headache, hemoptysis, pharyngitis, splenomegaly | patchy hilar infiltrates |
Pleural effusions are generally encountered in staphylococcal or streptococcal pneumonia.26 Gram-negative and anaerobic infections can cause effusions, which develop later in the course of the pneumonia.26 In these cases, the effusions frequently represent empyema.27 Occasionally, patients with Legionnaires’ disease, viral pneumonia, or Mycoplasma pneumonia may develop a small effusion.28,29
Lung abscesses are a rare complication of CAP. When they occur, they are generally secondary to Staphylococcus aureus or Klebsiella pneumoniae.27 Most pneumonias tend to occur in the lower lobe. Lobar infiltrates are associated with a number of bacteriologic etiologies, with pneumococcal pneumonia being the most common cause of lobar pneumonia. Klebsiella can also cause a lobar consolidation, particularly in association with a bulging fissure and empyema.30 Sublobar, unifocal consolidation can also occur with pneumococcal pneumonia and viral pneumonia, although it is not a common presentation for these entities.31
Chlamydia TWAR (or C. pneumoniae) is almost always unifocal in presentation. Multifocal infiltrates are the usual presentation of Staphylococcal pneumonia.32 Gram-negative infection, anaerobic infection, Mycoplasma pneumonia, and viral infections, as well as Legionella, also are common causes of multifocal infiltrates.32-34 Pulmonary infections may present as single or multiple lung masses. The so-called "round" infiltrate of pneumococcal and staphylococcal pneumonia occurs as a result of spread of infection from a single focus.35,36 Rarely, Legionella may also present with a mass-like appearance.31 Q fever and tularemia also may present with multiple, discreet masses.32,37,38 Cavitary lesions usually are the result of anaerobic abscesses, Staphylococcus aureus, or Gram-negative organisms such as Klebsiella or Pseudomonas.25,32 Cavitary lesions may occur in patients with psittacosis, although even in this disease it occurs only in 10%. Rarely, cavitation may be caused by Legionella.38 Interstitial or nodular infiltrates are seen in patients with psittacosis, Mycoplasma pneumonia, Pneumocystis carinii pneumonia (PCP), or viral pneumonia.39,40
Many studies on the etiology of CAP have focused on in-patients. Recent investigations emphasize that the spectrum of pathogens responsible for infection in ambulatory patients is different from that in patients ill enough to require hospitalization. In hospitalized patients, multiple agents are found in up to 42%, while an etiologic agent cannot be confirmed in about 38% of cases.41 Pneumococcus is the most commonly identified pathogen, followed by M. pneumoniae, Chlamydia pneumoniae, Legionella, and viral disease. Older patients and those with co-morbid disease are more likely to have bacterial causes of their pneumonia as compared to the higher incidence of atypical agents in younger patients. The etiology of pneumonia may also reflect the underlying immune status of the patient population. In inner city hospitals associated with a high incidence of AIDS, Pneumocystis carinii is a common etiologic agent.42 Pneumonia caused by atypical agents is less common in this patient population. In typical ambulatory settings, pneumonia caused by atypical agents may occur in as many as one-third of patients.43
Pneumococcal Pneumonia. Streptococcus pneumoniae remains the most common etiologic agent identified in patients with CAP.44,45 Pneumococcal pneumonia affects all age groups but is more common in children and the elderly. Patients with altered mucociliary clearance, such as smokers, alcoholics, and patients recovering from viral infection are also at higher risk for developing pneumococcal infection.46 Of note, patients at risk for pneumococcal pneumonia should be vaccinated. The risk for acquiring complications of pneumonia is reduced by two-thirds following vaccination.47 Similarly, yearly influenza immunization reduces the risk of both pneumococcal and other forms of bacterial pneumonia.48
In young children, pneumococcal pneumonia affects about 1:1000 children, while, in the elderly, pneumococcal pneumonia affects about 1:2000 patients.46 Otherwise healthy adults may develop pneumococcal pneumonia, particularly during epidemics occurring in crowded situations, although atypical agents are a more frequent cause of pneumonia in this population. Patients at particular risk for pneumococcal pneumonia include alcoholics, cigarette smokers, patients with chronic lung disease, patients with congestive heart disease, diabetics, individuals with cancer, those infected with the HIV virus, and patients who are otherwise immunosuppressed.49,50
The classical presentation of pneumococcal pneumonia consists of sudden onset of rigors, fever, cough, pleuritic chest pain, and rust colored sputum. This occurs more commonly in young patients and frequently is associated with a segmental or lobar pneumonia. Parapneumonic pleural effusions are common in this setting, occurring in about 25% of patients. Empyema is relatively uncommon, although about 10% of pleural effusions will evolve into an empyema.51,52 Bacteremia occurs commonly in pneumococcal pneumonia, particularly in patients who have asplenism or HIV infection.52 Bacteremia is associated with a higher mortality rate. Meningitis is an uncommon complication of pneumococcal pneumonia, although this diagnosis should be considered in patients with confusion or severe headache. Lung abscesses are a rare complication of pneumococcal pneumonia, as is purulent pericarditis.52
Atypical presentations must be appreciated by the clinician. In this vein, elderly patients, those with chronic lung disease, and individuals recovering from influenza may have a more insidious presentation of pneumonia. In this setting, the disease may be heralded by a mild cough, scant sputum production, or possibly by a change in sputum color and signs of dehydration. Pleural effusion is uncommon in this setting. Finally, patients who have functional or anatomic asplenism, transplant patients, or patients who have hypogammaglobulinemia may undergo a rapidly progressive course with high temperatures, hypotension, DIC, and multisystem organ failure.
Findings on the chest radiograph in patients with pneumococcal pneumonia are variable. Patients with so-called "classic" disease frequently have lobar or segmental pneumonia, while a patchy bronchopneumonia is a more characteristic finding in elderly patients. As noted above, pleural effusions are a common finding in pneumococcal pneumonia.26 Most patients with pneumococcal pneumonia will have a leukocytosis.46 Elevation of serum bilirubin or other liver enzymes may also occur.
There is a significant incidence of pneumococcal resistance to tetracycline and trimethoprin-sulfamethoxazole, particularly in children attending day care.54 Overall, macrolide resistance to pneumococci is about 9-11% in the United States.55 A macrolide such as azithromycin should be used for outpatient treatment. Other advanced generation macrolides or extended spectrum quinolones also may be considered. Clindamycin, while effective against pneumococcus is associated with a high incidence of adverse reactions. In the case of a patient with demonstrated high-level resistance or with severe infection, vancomycin, 1 gm intravenously every 12 hours is indicated.
Staphylococcus aureus. Staphylococcus aureus is an infrequent cause of CAP. It is more likely to occur in patients with COPD, patients with bronchogenic or laryngocarcinoma, patients with preceding viral illness, immunosuppressed patients, as a consequence of seizures, and in nursing home patients.55 Seeding of the lung by hematogenous spread is an occasional complication of intravenous drug abuse. Patients typically present with gradual onset fever, purulent sputum, and dyspnea, although rarely there may be a more dramatic and aggressive onset of the disease.56 The chest radiograph usually demonstrates empyema and pleural effusions, accompanied by multi-lobar infiltrates; abscess formation may also occur with S. aureus pneumonia. Patients with S. aureus pneumonia will require admission for treatment with penicillinase resistant antibiotics and, in some cases, with vancomycin.
Klebsiella pneumoniae. Klebsiella pneumonia occurs primarily in alcoholics, nursing home patients, and occasionally in patients with COPD. Almost all cases occur in patients older than 40 years. The onset is generally sudden and associated with cough, sputum production, rigors, malaise, and pleuritic chest pain. The sputum of patients with Klebsiella pneumonia is thick and bloody with a currant jelly appearance. Herpes labialis occurs in about 10% of patients with Klebsiella pneumonia.57 The characteristic chest radiograph shows a lobar pneumonia, bulging fissures, and occasionally, abscess formation.58 Treatment usually includes a third-generation cephalosporin or an extended spectrum quinolone with or without an aminoglycoside. An extended spectrum penicillin such as ticarcillin/clavulinic acid may also be effective.
Pseudomonas. Pseudomonas pneumonia is responsible for a rapidly progressive and severe disease. Patients are frequently toxic in appearance, confused, and cyanotic.57 A relative bradycardia may occur. Empyema is common, along with bilateral lower lobe streaky infiltrates. The mortality rate ranges up to 80%.59 Pseudomonas infection should be considered in the seriously ill, hospitalized patient.
Hemophilus influenzae. H. influenzae occurs both in children and in adults. Adults with this form of pneumonia tend to have underlying pulmonary disease such as carcinoma, COPD, or chronic alcoholism.60 Occasionally, the elderly, diabetics, immunocompromised patients, and those with sickle cell anemia may develop H. influenzae infection. Immunization has decreased the incidence of H. influenzae infection in children. Patients usually present with a fairly abrupt course characterized by fever, cough, sputum production, chest pain, and dyspnea. Bacteremia has been a common finding in Hemophilus pneumonia in children in the past, and may also occur in patients older than age 50. (See Table 4.) The chest radiograph usually demonstrates a multi-lobar pattern.60 Pleural effusions are seen in about one-half of patients.
| Table 4. Etiologic Agents of Pneumonia in Children | ||||
| Neonate | ||||
| Group B Streptococcus | ||||
| Listeria monocytogenes | ||||
| Gram negatives—E. coli, Klebsiella | ||||
| Chlamydia trachomatis (neonate to 3 months) | ||||
| Cytomegaloviris | ||||
| Herpes simplex virus | ||||
| Rubella virus | ||||
| < 1 year | ||||
| Streptococcus pneumoniae | ||||
| Haemophilus influenzae | ||||
| Staphylococcus aureus | ||||
| Respiratory syncytial virus | ||||
| Parainfluenza virus | ||||
| > 1 year | ||||
| Streptococcus pneumoniae | ||||
| Haemophilus influenzae | ||||
| Staphylococcus aureus | ||||
| Influenza virus | ||||
| Rhinovirus | ||||
| Parainfluenza virus | ||||
| Adenovirus | ||||
| Enterovirus | ||||
| Varicella virus | ||||
| Epstein-Barr virus | ||||
| Chlamydia penumoniae (school-age) | ||||
| Mycoplasma pneumoniae (school-age) | ||||
Legionella. Legionella pneumophila was recognized as a causative agent in pneumonia following the epidemic at the 1976 American Legion Convention.61 A variety of species of Legionella can cause pneumonia, although Legionella pneumophila, sera group 1, is by far the most common causative agent.62 Legionella species are found in water sources, including rivers, cooling towers, and hot water tanks. The organism is pleomorphic and faintly gram negative.63 Patients at risk for Legionnaires’ disease include patients with a history of cigarette smoking, COPD, and immunosuppression.64,65 Transplant patients are also at significant risk for Legionella pneumonia following surgery.66 Although Legionella is commonly thought of as a disease of older patients, it can be seen in pediatric patients, particularly in immunosuppressed patients, post operatively, and in the neonatal period.67,68
Legionella infection can be seen at any time of the year; however, bacterial pneumonia is more common in the winter, while Legionella is a more common cause of pneumonia during the summer months. Legionella can cause a range of pulmonary disease from a benign, self-limited illness manifested by cough and low-grade fever to acute respiratory distress and multi-system failure. A brief illness with fever, malaise, and headache is sometimes termed Pontiac fever.69 Shaking chills are common in patients with Legionella.70 Pleuritic chest pain and hemoptysis, although not common, may mimic pulmonary embolism. Gastrointestinal symptoms such as abdominal pain, nausea, vomiting, and watery diarrhea may occur.70
Legionella also can cause extra-pulmonary symptoms, including sinusitis, cellulitis, pancreatitis, peritonitis, palnephritis, and myocarditis.71,72 Although hyponatremia is encountered in a number of pneumonias, it occurs more commonly in Legionella.62,69 There is no consistent pattern to the white blood count, although patients are more likely to have a leukocytosis than a leukopenia. A mild elevation of liver enzymes can also be seen.62 The chest radiograph frequently shows a patchy localized infiltrate. Lower lobe infiltrates and hilar adenopathy may also occur. Pleural effusions are seen in one-third of patients,70 and immunosuppressed patients may demonstrate cavitary lesions.73
Legionella is sensitive to macrolide antibiotics; because erythromycin is associated with a high incidence of side effects,15 azithromycin is the macrolide of choice, and may be given intravenously. The quinolone antibiotic levofloxacin also is effective. Additional antibiotics that demonstrate activity include tetracyclines, sulfonamide, clindamycin, and imipenem.74 Rifampin should be added to patients who fail to demonstrate a prompt clinical response.
Moraxella catarrhalis. Moraxella catarrhalis is a respiratory pathogen that is most likely to cause infection in patients with underlying COPD. However, it also occurs occasionally in patients with other chronic diseases, such as diabetes mellitus, congestive heart failure, lung cancer, or cerebral vascular diseases.75 Patients typically have a one-week prodromal syndrome of bronchial infection with cough and sputum production. In pediatric patients, Moraxella may cause otitis media, sinusitis, or conjunctivitis.76 Most cases occur during the winter months. Moraxella frequently occurs in combination with H. influenzae and Streptococcus pneumoniae.77 Fever occurs in most, although not all patients.78 Pleuritic chest pain occurs in about one-half of patients.75 The chest radiograph typically demonstrates diffuse infiltrates, although occasionally lobar consolidation may occur. Moraxella catarrhalis responds to macrolide antibiotics, tetracycline, trimethroprim/sulfamethoxalone, extended spectrum penicillins, beta-lactam/lactamase inhibitors, second and third generation cephalosporins, and quinolone antibiotics. Patients with Moraxella catarrhalis frequently have indications for admission.
Chlamydia pneumoniae. Chlamydia pneumoniae or Chlamydia TWAR is a respiratory pathogen that exists as an obligate intracellular bacteria. C. TWAR infections are common, and almost 50% of the population has antibodies indicating prior infection.79 It appears that most patients who have antibodies to Chlamydia develop them between the ages of 5 and 14.80 Most patients with Chlamydia infection have only mild symptoms of respiratory illness which may include sore throat, hoarseness, and a cough that develops a week after the onset of symptoms. Early in the course of illness, patients have a fever that remits after several days.81 Rales or rhonchi are frequent findings on physical examination.81 Sinusitis may be associated with Chlamydia pneumonia. Most patients have a subsegmental focal infiltrate, and pleural effusions are rarely seen.82 Older individuals may have more extensive findings, including multifocal infiltrates or pleural effusions.82
Chlamydia pneumoniae responds to a number of antibiotics, including macrolides and extended spectrum quinolones such as azithromycin and levofloxacin, which demonstrate effective coverage against Chlamydia as well as Mycoplasma and Legionella.12 Penicillins and trimethroprim/sulfamethoxazone are not effective.
Mycoplasma pneumoniae. Mycoplasma pneumoniae is a gram-negative aerobe that lacks a cell wall. It is a common causative agent of pneumonia in children and young adults. Mycoplasma pneumonia occurs year round and since other causes of bacterial pneumonia occur in the winter, it, along with Legionella, will be a more common cause of pneumonia in the summer months. Mycoplasma pneumonia occurs in epidemics every 4-8 years,82 and it tends to cause a relatively mild respiratory illness. Most patients will have cough, malaise, chills, pharyngitis, and headache. Many patients will have symptoms consistent with a upper respiratory infection, including rhinorrhea and earache. Patients with Mycoplasma infection frequently do not develop pneumonia. Retrosternal chest pain associated with cough and deep breathing is a common finding.83 GI symptoms are rare in Mycoplasma pneumonia.
Mycoplasma pneumonia has a varied radiographic presentation which may include unilateral infiltrates, patchy multifocal infiltrates, or bilateral infiltrates. About 20% of patients will have hilar adenopathy.28 Additionally, about 20% of patients will have small pleural effusions.28 Mycoplasma pneumonia tends to be more severe in patients with sickle cell disease.84 Sinusitis is found in about two-thirds of patients with Mycoplasma pneumonia.85 Rarely, patients may have extrapulmonary complications, including hemolytic anemia, DIC, and renal failure. A significant minority of patients will have skin rashes.86 Rarely, patients may have neurologic symptoms, including encephalitis, transverse myelitis, and radiculopathies. Since Mycoplasma lacks a cell wall, penicillins and cephalosporins will not be effective against this disease. Antibiotics may reduce the duration of illness.
Unusual Causes of Community-Acquired Pneumonia
Although viral infection, pneumonococcal pneumonia, H. influenzae, M. catarrhalis, Mycoplasma pneumoniae, Chlamydia TWAR, and Legionella account for the majority of patients with CAP, some additional agents may be considered in certain settings.
Group A Streptococcus. Group A streptococcal infection is most often associated with pharyngitis and rheumatic fever. Group A streptococcal pneumonia may occur after viral illness, particularly in toddlers and young people living in close quarters.87 These patients present with abrupt onset of fever, shortness of breath, and chest pain. Empyema is a common finding in these patients.
This organism has generally been associated with perinatal infection. Pneumonia caused by this agent usually occurs in older debilitated patients with underlying co-morbid disease.88 The clinical presentation is associated with hypotension, tachycardia, and tachypnea. This organism is frequently associated with other pathogenic bacteria.
Enterococcus. In the past, group D streptococci was associated with pneumonia in elderly and/or chronically ill medical patients. Pneumonia secondary to this agent is associated with the presence of feeding tubes and institutionalization.89
Acinetobacter. This organism is ubiquitous in the environment and colonizes the skin in 25% of normal patients. CAP from this agent may occur in alcoholics, patients undergoing renal dialysis, patients with COPD, or other chronically ill patients.90 Pneumonia due to Acinetobacter is frequently associated with severe respiratory distress, pleural effusions, and abscess formation.91
Listeria. Listeria is another organism that is common to the environment and is frequently carried by asymptomatic patients. It is also associated with perinatal infection and infection in immunocompromised patients. The most common setting in which this organism is found is in patients with underlying hematologic malignancies.92 Pleural effusions are common with pneumonia secondary to this agent.
Bacillus cerius. This organism is usually associated with food poisoning; however, it may cause pneumonia in alcoholic patients. Most patients with Bacillus cerius pneumonia will have hemoptysis.93 Eikenella corrodens is also associated with pneumonia in alcoholics. These patients have cavitary lesions and pleural effusions.
Hanta virus. Hanta virus is carried by rodents. There was a high incidence of infection with this virus among military personnel in Korea, where the disease was known Korean hemorrhagic fever.94 Most recently, this infection has been associated with an outbreak in the Southwest United States, although cases have been found east of the Mississippi River. In areas that are reservoirs for Hanta virus, the disease may be suspected on the basis of the development of adult respiratory distress syndrome or bilateral pulmonary infiltrates in previously healthy persons without underlying medical illness.
Q Fever. Most patients who develop Q fever have a benign febrile illness lasting several days to two weeks; it is usually characterized by malaise, myalgia, and severe headache.95 Patients with Q fever and pneumonia will generally have a non-productive cough and diaphoresis. The disease may occur with sudden onset of chills and high fever, is caused by Coxiella burnetii, and occurs as a result of exposure to livestock, drinking unpasteurized milk, exposure to parturient cats, or via tick bite.96 Q fever can also present with more serious manifestations, including endocarditis, meningitis, osteomyelitis, hemolytic anemia, and hepatitis.
Pneumonia occurs occasionally in Q fever and may be associated with epidemics. Most patients have a mild to moderate pneumonia. On physical examination, inspiratory crackles may be heard. Rarely, patients may have splenomegaly. The chest x-ray occasionally shows lobar consolidation, but more usually reveals a rounded segmental lower lobe densities.36,97 Doxycycline is felt to be an effective form of treatment for this disease and is administered in doses of 100 mg, twice a day, for 10 days. Macrolide antibiotics, quinolones, rifampin, chloramphenicol, and trimethroprim may also be effective.98
The Immunocompromised Patient
Patients may be immunocompromised for a number of reasons, including HIV infection, immunosuppression in transplant patients, chronic steroid use, functional asplenism secondary to sickle cell disease, or treatment of malignancy. This section will focus primarily on the spectrum of pulmonary infections encountered in the HIV patient. A number of infectious processes are associated with HIV infection. Although a variety of bacterial infections can occur in the HIV patient, Streptococcus pneumoniae is still the most common etiologic agent causing CAP. (See Table 5.) The annual incidence of pneumonia is about 1%, or 5 times the rate in seronegative patients.99
| Table 5. Etiologic Agents of Pneumonia in the Immunocompromised Patient | ||||
| Bacterial | ||||
| Streptococcus pneumoniae | ||||
| Haemophilus influenzae | ||||
| Staphylococcus aureus | ||||
| Pseudomonas aeruginosa | ||||
| Klebsiella pneumoniae | ||||
| Legionella pneumophilia | ||||
| Mycoplasma pneumoniae | ||||
| Fungal | ||||
| Histoplasmosis capsulatum | ||||
| Coccidioidomycosis immitis | ||||
| Blastomycosis dermatitidis | ||||
| Cryptococcus neoformans | ||||
| Aspergillis | ||||
| Other | ||||
| Mycobacterium tuberculosis | ||||
| Mycobacterium avium complex | ||||
| Pneumocystis carinii | ||||
| Cytomegalovirus | ||||
| Influenza virus | ||||
| Adenovirus | ||||
With the onset of the AIDS epidemic in the 1980s, the differential diagnosis of pneumonia was expanded to include agents formerly seen only on an infrequent basis. Foremost among these agents is Pneumocystis carinii, a protozoan with a low degree of virulence for healthy, immunocompetent hosts. PCP is the most common cause of death in the AIDS patient and carries a 5-10% mortality rate for the first episode.100 The presentation of PCP is often insidious, with a gradually worsening, non-productive cough, dyspnea on exertion, and weight loss. Patients may have symptoms for as long as a month. Fever may be absent in up to 20% of cases, and symptoms may progress over the course of several weeks. A chest x-ray typically shows bilateral perihilar interstitial infiltrates, but consideration variation can be seen. Up to 20% of patients presenting with PCP lack radiographic findings on the initial chest radiograph.101
If the HIV status of the patient is not known, but the individual has positive risk factors or evidence of opportunitistic infection, PCP must be considered as a cause for any respiratory complaints. If the patient is known to have HIV, the most recent CD4 lymphocyte count is useful in ascertaining the risk of opportunistic pulmonary infection. Studies have shown that a CD4 count less than 200/mm3 is more common in patients presenting with PCP.102 LDH levels greater than 220 IU have also been shown to be associated with PCP infection.103 Definitive diagnosis requires sputum induction and silver staining. Invasive procedures may be required to obtain an adequate specimen. Given the time required for pathogen confirmation, cases are usually admitted for presumptive antibiotic therapy while awaiting diagnostic test results. Antibiotic therapy includes IV TMP/SMX or pentamidine. These agents are also used as outpatient prophylaxis for PCP. Either daily single-dose TMP/SMX or a monthly dose of aerosolized pentamidine are accepted therapeutic options. Intravenous steroids may also be used for moderate to severe cases of PCP. Recent reports, however, have proposed a rule for outpatient management plan for outpatient treatment of pneumonia in HIV-positive patients. The sulfamethoxazole/ trimethroprim (TMP/SMX) combination that is used for PCP prohphylaxis generally—but not always—is effective for suppressing PCP, as well as pneumonias caused by other etiologies.
Consequently, the emergence of a bacterial or atypical pneumonia in an HIV-positive individual who is on prophylactic TMP/SMX should raise the clinician’s index of suspicion for: 1) infection with a resistant species of Streptococcous pneumoniae; 2) infection with a virulent, potentially gram-negative or atypical pathogen against which TMP/SMX may not show sufficient activity; or 3) significant immunocompromise, suggesting the need for aggressive in-hospital management. As a result, outpatient treatment of pneumonia in HIV-positive patients probably should be reserved for individuals who either: 1) are not on TMP/SMX prophylaxis, or 2) are taking a PCP prophylaxis regimen that does not include TMP/SMX.104
To qualify for outpatient management, the patient should also have reasonable oxygenation (i.e., PO2 > 70 mmHg or an O2 saturation > 95%), and the chest x-ray should be consistent with PCP, that is, it should show a pattern of diffuse, interstitial infiltrates. Because a definitive radiological diagnosis of PCP is not always possible, and because PCP can be confused with lower respiratory tract infections caused by bacterial or atypical pathogens, outpatient treatment of patients with HIV-positive status should consist of TMP/SMX in combination with a macrolide (i.e., azithromycin) or an extended spectrum quinolone (levofloxacin). If the patient does not improve within two days, then admission to the hospital is indicated.
As might be expected, bacterial pneumonias are also commonly encountered in the HIV patient. As with the general adult population, the most common pathogens are S. pneumoniae and H. influenzae,105 with studies showing that S. pneumoniae accounts for about 34-58% of confirmed cases of bacterial pneumonia in HIV-positive individuals.105 Overall, the incidence of S. pneumoniae pneumonia has been found to be approximately 7-10 times greater in the HIV infected population,106 and one study has shown the incidence of H. influenzae to be up to 100 times higher in this high-risk subgroup.107 Pneumonia caused by Staphylococcus aureus also occurs more commonly in the HIV-positive patient, with a reported incidence among pneumonia patients as high as 23%.108
Etiologic diagnosis can be complicated by atypical radiographic findings in this patient population. For example, bacterial pneumonia may present with an interstitial infiltrate pattern, instead of the more common lobar infiltrate characteristic of bacterial infection.109 In addition, patients with HIV infection are more likely to have multilobar infiltrates and their clinical course is more likely to be complicated by bacteremia.110 These adverse clinical features may influence patient disposition (i.e., encourage the clinician to manage the patient in the hospital) and choice of antibiotics.
It should be stressed that the immunocompromised host has an increased likelihood of acquiring pulmonary TB and is at risk for infection with other mycobacterial species (M. avium complex). Chest x-ray findings are not always helpful for establishing a definitive TB diagnosis in this population, and skin testing may reveal an anergic response. Patients should be placed in respiratory isolation until TB can be ruled out by acid-fast staining or culture of respiratory secretions.
The Elderly Patient
As has been emphasized throughout this article, the older individual with a lower respiratory tract infection represents a high-risk subgroup that is of special concern. Not surprisingly, this patient population has a higher incidence of coexisting disease, such as diabetes, CHF, CAD, chronic lung disease, renal insufficiency, chronic alcoholism, and neoplasms. The presentation of CAP in the geriatric patient can also be atypical. Compared to younger adults, the elderly are less likely to have pleuritic chest pain, hemoptysis, cough, or dyspnea as a manifestation for pneumonia.2 Moreover, this patient subgroup is more likely to present with dyspnea, and the duration in symptoms prior to diagnosis is longer for patients older than age 75 compared to younger adults.
The site or environment where patients acquire CAP and their history regarding lower respiratory tract infections can influence antibiotic selection. For example, elderly patients may present from a nursing home, or they may have been recently hospitalized. These historical features increase the likelihood of infection with nosocomial pathogens such as Klebsiella pneumoniae and Pseudomonas aeruginosa. Accordingly, initial antibiotic selection in the emergency department would, from an appropriate intensity and spectrum-of-coverage perspective, include agents indicated for CAP caused by these organisms. An effective option would include a fluoroquinolone such as ciprofloxacin; however, if there is a high likelihood of Pseudomonas infection, it would be prudent to add an antipseudomonal beta-lactam (carbapenem or cefepime) or an aminoglycoside.
Chronic alcoholism and stroke predispose to aspiration pneumonia. Anaerobic sources of infection (i.e., Bacteroides fragilis) must be considered in these patients, and initial choices should reflect this concern.111 Spectrum-sensitive coverage for these patients would include clindamycin or a beta-lactam/beta-lactamase inhibitor.
A supportive home environment with close physician follow-up will optimize chances for successful treatment. For patients who live alone or in an unstable home environment, who have several concomitant medical problems, who have underlying nutritional compromise, or for whom compliance with medical treatment is a concern, admission for treatment is warranted. This is especially applicable if the patient presents with progonositically adverse laboratory abnormalities or physical findings, such as fever higher than 40°C, pulse higher than 125/min, respiratory rate greater than 30/min, hypotension, or hypoxia.112
The importance of early identification and treatment of pneumonia in elderly patients cannot be overemphasized. In a large analysis of 4069 patients older than age 65,104 the overall 30-day mortality rate was 15%. Most importantly, early administration of antibiotics was shown to be associated with a lower mortality rate. Patients to whom antibiotics were administered more than 10 hours after arrival to the hospital were 20% more likely to die than those who had early administration of antibiotics.104
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Physician CME Questions
81. Community-acquired pneumonia (CAP) accounts for about how many adult hospitalizations per year?
A. 100,000
B. 200,000
C. 300,000
D. 400,000
E. 500,000
82. According to one study with 4069 patients, the overall 30-day mortality of patients older than 65 was:
A. 5%.
B. 10%.
C. 15%.
D. 20%.
E. 25%.
83. The most common etiology identified in patients with CAP is:
A. S. pneumoniae.
B. L. pneumophilia.
C. E. coli.
D. Klebsiella.
E. none of the above.
84. Chronic stroke and alcoholism predispose a patient to:
A. Mycoplasma pneumonia.
B. Aspiration pneumonia.
C. viral pneumonia.
D. none of above.
85. Typical symptoms of a patient presenting with Streptococcus pneumoniae include:
A. pleuritic chest pain.
B. bloody sputum.
C. GI disturbance.
D. Both A and B.
86. Legionella pneumonia is most commonly seen during:
A. fall months.
B. summer months.
C. winter months.
D. spring months.
87. Staphylococcous aureus pneumonia is more likely to occur in:
A. patients with COPD.
B. patients with bronchogenic carcinoma.
C. patients with preceding viral illness.
D. nursing home patients.
E. all of above.
88. Pneumococcal pneumonia is:
A. more common in middle-age adults.
B. more common in neonates.
C. more common in children and elderly.
D. none of above.
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