Pneumonia remains one of the leading causes of morbidity and mortality in the United States, especially in older adults, young children, and those with underlying chronic disease or immunocompromise. In primary care practice, two of the most important issues related to pneumonia are awareness of the common infectious pathogens and their treatment and decisions regarding the appropriateness of outpatient treatment. This course will provide the diagnostic criteria of the disease and discuss the pathology of several different bacteria strains responsible for pneumonia. The evidence-based guidelines for the treatment and prevention of pneumonia will be explored, and the course will end with a discussion of sick-day management and patient education needs.

Education Category: Infection Control / Internal Medicine
Release Date: 06/01/2015
Review Date: 05/01/2018
Expiration Date: 08/31/2018


This course is designed for nurses and allied healthcare professionals involved in the diagnosis and treatment of pneumonia.

Accreditations & Approvals

In support of improving patient care, NetCE is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team. NetCE is approved by the California Nursing Home Administrator Program as a provider of continuing education. Provider number 1622. NetCE is approved to offer continuing education through the Florida Board of Nursing Home Administrators, Provider #50-2405. NetCE is accredited by the International Association for Continuing Education and Training (IACET). NetCE complies with the ANSI/IACET Standard, which is recognized internationally as a standard of excellence in instructional practices. As a result of this accreditation, NetCE is authorized to issue the IACET CEU. NetCE is approved as a provider of online continuing education for certified nursing assistants through the California Department of Public Health Licensing and Certification Division. Nurse Aide Certification (NAC) Provider #7005. This program has been pre-approved by The Commission for Case Manager Certification to provide continuing education credit to CCM® board certified case managers. The course is approved for 10 CE contact hour(s). Activity code: H00029568. Approval Number: 170004573. To claim these CEs, log into your CE Center account at www.ccmcertification.org.

Designations of Credit

NetCE designates this continuing education activity for 10 ANCC contact hour(s). NetCE designates this continuing education activity for 4 pharmacotherapeutic/pharmacology contact hour(s). NetCE designates this continuing education activity for 12 hours for Alabama nurses. This home study course is approved by the Florida Board of Nursing Home Administrators for 5 credit hour(s). This course is approved by the California Nursing Home Administrator Program for 10 hour(s) of continuing education credit - NHAP#1622010-6471/P. California NHAs may only obtain a maximum of 10 hours per course. AACN Synergy CERP Category A. NetCE is authorized by IACET to offer 1 CEU(s) for this program.

Individual State Nursing Approvals

In addition to states that accept ANCC, NetCE is approved as a provider of continuing education in nursing by: Alabama, Provider #ABNP0353, (valid through November 21, 2017); Alabama, Provider #ABNP0353, (valid through November 21, 2021); California, BRN Provider #CEP9784; California, LVN Provider #V10662; California, PT Provider #V10842; District of Columbia, Provider #50-2405; Florida, Provider #50-2405; Georgia, Provider #50-2405; Iowa, Provider #295; Kentucky, Provider #7-0054 through 12/31/2019; South Carolina, Provider #50-2405.

Course Objective

The purpose of this course is to provide healthcare professionals with the information necessary to appropriately diagnose and treat patients with pneumonia in order to decrease the associated morbidity and mortality and public health strain.

Learning Objectives

Upon completion of this course, you should be able to:

  1. Outline the definition and epidemiology of pneumonia and its impact on public health.
  2. Describe the pathophysiology of pneumonia.
  3. List risk factors for pneumonia infection.
  4. Analyze the various pneumonia syndromes, including bacteria syndromes, atypical syndromes, and Legionnaires' disease.
  5. Use diagnostic criteria to appropriately identify and categorize pneumonia.
  6. Describe the key aspects of antibiotic therapy for pneumonia, including considerations for resistant organisms, adherence to therapy, and duration of treatment.
  7. Appropriately refer pneumonia patients in need of inpatient care.
  8. Provide patients and/or their families with information regarding appropriate sick-day management, transmission prevention, and medication adherence.
  9. Discuss strategies to prevent bacterial healthcare-associated pneumonia.
  10. Identify potential complications of pneumonia in various patient populations, including infection with multidrug-resistant organisms.


Carol Whelan, APRN, has been working in nursing education since 2000. She received her Master's degree in psychiatric/mental health nursing from St. Joseph College in West Hartford, Connecticut, and completed post-graduate nurse practitioner training at Yale University. Ms. Whelan is an Associate Clinical Professor and Lecturer at Yale University and works as an APRN at the Department of Veterans' Affairs in Connecticut, where she also serves as the Vice President of Medical Staff. She has authored many articles, textbook chapters, and books.

Faculty Disclosure

Contributing faculty, Carol Whelan, APRN, has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

Division Planner

Jane C. Norman, RN, MSN, CNE, PhD

Division Planner Disclosure

The division planner has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

About the Sponsor

The purpose of NetCE is to provide challenging curricula to assist healthcare professionals to raise their levels of expertise while fulfilling their continuing education requirements, thereby improving the quality of healthcare.

Our contributing faculty members have taken care to ensure that the information and recommendations are accurate and compatible with the standards generally accepted at the time of publication. The publisher disclaims any liability, loss or damage incurred as a consequence, directly or indirectly, of the use and application of any of the contents. Participants are cautioned about the potential risk of using limited knowledge when integrating new techniques into practice.

Disclosure Statement

It is the policy of NetCE not to accept commercial support. Furthermore, commercial interests are prohibited from distributing or providing access to this activity to learners.

Table of Contents

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#34671: Pneumonia

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Pneumonia remains one of the leading causes of morbidity and mortality in the United States, especially in older adults, young children, and those with underlying chronic disease or immunocompromise. Although the list of organisms causing pneumonia is long and increasing, relatively few organisms are responsible for most cases of pneumonia. In primary care practice, two of the most important issues related to pneumonia are awareness of the common infectious pathogens and their treatment and decisions regarding the appropriateness of outpatient treatment. The purpose of this course is to provide healthcare professionals with the information necessary to diagnose and treat patients with pneumonia in order to decrease the associated morbidity and mortality and public health strain. This course will provide the diagnostic criteria of the disease and discuss the pathology of several different bacteria strains and other pathogens responsible for pneumonia.


Hippocrates first described the clinical picture of pneumonia in 400 B.C.E., including the presence of fever, chest pain, productive cough, rales, and dyspnea [1]. However, the disease was recognized even before Hippocrates' time. The disease has resulted in a serious public health and mortality burden over the years, with Osler referring to pneumonia as the "captain of the men of death" in the early 1900s [2]. During this same period, pneumonia surpassed tuberculosis as a leading cause of death.

However, dramatic changes in the past century, namely the introduction of effective antibiotics and vaccinations and improved medical and surgical techniques, have changed the clinical picture of pneumonia dramatically. These developments have resulted in vast improvements in morbidity and mortality from pneumonia in developed countries. But despite these advances, pneumonia remains a major health concern, and the emergence of multidrug-resistant organisms has led to renewed interest and research on this ancient disease.


Pneumonia is an infection of the lower respiratory tract that is usually accompanied by cough, fever, malaise, and chest x-ray abnormalities. Sputum production, dyspnea, hypoxia, and hemoptysis may be present in some individuals with pneumonia, depending on the causative organism. The disease is further classified as community-acquired, healthcare-associated, or hospital-acquired according to how and where it was contracted.

The Infectious Diseases Society of America (IDSA) defines community-acquired pneumonia (CAP) as an acute infection of the pulmonary parenchyma frequently associated with at least two symptoms of active infection occurring in individuals who have not been hospitalized or resided in a long-term care facility for 14 days before the onset of symptoms [3]. In most cases of CAP, diagnosis is made by history and physical examination; identification of the etiologic agent is usually not necessary. Although the list of organisms causing CAP is long and increasing, relatively few organisms are responsible for most cases of pneumonia.

Hospital-acquired pneumonia is defined as any pneumonia in a patient who has been hospitalized 48 hours prior to onset of symptoms and that was not incubating prior to admission [4]. Ventilator-associated pneumonia refers to a pneumonia that develops at least 48 hours after intubation and the initiation of mechanical ventilation. An additional subtype of pneumonia is healthcare-associated pneumonia, which refers to pneumonia in patients who are not hospitalized but have had contact with the healthcare system. A further subgroup of healthcare-associated pneumonia is nursing home-associated pneumonia. An important factor in treating healthcare-associated and hospital-acquired pneumonias is the recognition that the causative organisms are generally more resistant to first-line antibiotics.

Multidrug-resistant bacterial pathogens are very often a cause of healthcare-associated, hospital-acquired, and ventilator-associated pneumonias. Pathogens responsible for multidrug-resistant pneumonias can include Pseudomonas aeruginosa, Acinetobacter spp., and methicillin-resistant Staphylococcus aureus (MRSA).

Aspiration pneumonia is an infectious process caused by inhalation of oropharyngeal secretions that are colonized with bacteria. Aspiration pneumonia is distinct from aspiration pneumonitis (caused by the inhalation of sterile gastric contents), but the syndromes can overlap. This type of pneumonia is a major cause of morbidity and mortality in both nursing home residents and hospitalized patients [5].

Atypical pneumonia is a term used to refer to pneumonia caused by bacteria and nonbacterial organisms that do not share characteristics commonly found in patients with pneumonia. Causative agents include Legionella spp., Mycoplasma pneumoniae, Chlamydophila spp., and Coxiella burnetii [4].

The treatment of pneumonia, both CAP and nosocomial, has been standardized to some degree by the publication of consensus guidelines by the IDSA and the American Thoracic Society [3,4]. The successful treatment of pneumonia depends on the correct empiric antibiotic selection and knowledge of its proven effectiveness in vivo. A working knowledge of the organisms that most commonly infect different age-groups and the habits or characteristics that put an individual at risk for specific etiologic agents is essential.

The most common cause of bacterial pneumonia is the gram-positive bacterium Streptococcus pneumoniae, estimated to be the cause of 20% to 60% of pneumonia cases [6]. Possible gram-negative infective organisms include Haemophilus influenzae, Klebsiella pneumoniae, and Moraxella catarrhalis. K. pneumoniae infections are more commonly diagnosed when there is co-existent alcoholism [3,4]. S. aureus and H. influenzae infections often occur after a primary influenza infection. M. catarrhalis, an organism not thought to be pathogenic, is most commonly found in those with chronic lung conditions, such as chronic obstructive pulmonary disease (COPD) [7]. It is also found in patients with diabetes, who are taking steroids, or who have other underlying chronic lung conditions or malignancy [7].

Another organism known to cause pneumonia is Legionella pneumophila. This organism was first implicated in 1976 after 182 people became ill in Philadelphia while attending an American Legion convention [8]. The organism is a gram-negative bacillus that survives in water and soil. Infection with the organism is acquired through inhalation of aerosolized droplets, making air-conditioning ventilating systems an obvious reservoir.

Potential atypical and nonbacterial organisms responsible for pneumonia include M. pneumoniae, Chlamydia pneumoniae (the Taiwan acute respiratory [TWAR] strain), and multiple viruses. Mycoplasma organisms lack cell walls and cannot be stained and visualized by conventional methods. Infection with these organisms usually causes disease in younger individuals and follows a milder course than that seen in patients with bacterial pneumonia. Chlamydial infection also manifests as a mild infection spread from person to person by aerosolized droplet secretions.

Pneumonia remains one of the leading causes of morbidity and mortality in the United States, especially in older adults and in those with underlying chronic disease. It is the leading cause of death from infectious disease and the eighth most common cause of death overall in the United States [9]. It is estimated that 4 million episodes of pneumonia are diagnosed in the United States every year, with a total of 30 million days of disability [10,11]. The World Health Organization (WHO) estimates that 57 million people die from pneumonia every year, with a bimodal distribution of mortality, with peaks in children younger than 5 years of age and adults older than 75 years of age [12]. Pneumonia killed an estimated 935,000 children younger than 5 years of age in 2013, with the majority of these deaths occurring in developing countries [12]. These are surprising statistics given the advent of broad-spectrum antibiotics, a multivalent pneumococcal vaccine, and sophisticated hospital care.

The elderly have the highest rates of CAP in the United States [13,14,15,16]. Aging is associated with a variety of declines in immune function (immune senescence) and prevalent comorbidities. As a result, the elderly constitute the largest immunocompromised population in the United States, putting them at risk for new infectious agents. Pathogens that are not typical causative agents of pneumonia must be considered as possible etiologic agents in the elderly. As a result, older adults are more likely to have CAP caused by a resistant organism or tuberculosis and to require hospital admission [17].

Clues to the specific cause of the pneumonia can be found in the patient's history. Enteric gram-negative bacilli, Pseudomonas organisms, and staphylococci are often found in patients who are hospitalized or live in nursing homes; other pathogens are associated with specific exposures and patient behaviors (Table 1).


Patient CharacteristicsPossible Pathogen(s)
Oral anaerobes
Streptococcus pneumoniae
Gram-negative bacilli
COPD, tobacco use
Haemophilus influenzae
S. pneumoniae
Moraxella catarrhalis
Nursing home resident
S. pneumoniae
Gram-negative bacilli
H. influenzae
Staphylococcus aureus
Poor dental hygieneOral anaerobes
Recent exposure to contaminated plumbing or waterLegionella organisms
Exposure to birds
Chlamydia psittaci
Histoplasma capsulatum (histoplasmosis)
HIV infection
Pneumocystis carinii
S. pneumoniae
H. influenzae
Mycobacterium tuberculosis
Exposure to excreta of wild rodentsSin nombre virus (hantavirus pulmonary syndrome)
COPD = chronic obstructive pulmonary disease.

The incidence of some pneumonias is linked to the season and the geographic area. Influenza illness in the winter increases the prevalence of secondary S. pneumoniae, S. aureus, and H. influenzae pneumonias. H. influenzae is known to have a short incubation period and moves through communities rather quickly. Mycoplasmal respiratory infection tends to move through communities slowly due to a longer incubation period and lower communicability. Legionella organisms have been known to infect a large number of people simultaneously from a single reservoir, so these outbreaks are often confined to a specific area [18].


The lungs are usually a sterile environment maintained by a host of natural defenses. The airways act as a filtration and humidification system for inspired air. Epithelial cells line the entire respiratory tract and contain cilia that constantly beat upward toward the pharynx. This action is a physical means of eliminating foreign material. Also, an intact gag reflex prevents the entry of particles, mucus, and food debris. Finally, the immune system is responsible for mechanisms, such as the action of phagocytes, macrophages, neutrophils, complement, and immunoglobulins, that retard advancement of pathogenic organisms that do gain access to this normally sterile environment.

Pneumonia often begins in the upper respiratory tract and gradually moves to the lower respiratory tract and proliferates. In order to do so, the infecting organism must overwhelm the natural host defenses, either due to the presence of risk factors or a compromised immune system. The infecting organism is generally introduced into the lungs via inhalation or aspiration; rarely, organisms may infect through the bloodstream. The progression of the disease depends on the type of infecting agent (e.g., virus, bacteria), but in all cases it is characterized by inflammation of the alveoli and terminal airspaces. Damage by the micro-organism and/or the host response results in air loss, consolidation, pulmonary edema, and crackles in lung sounds. In patients with viral infections, accumulation of white blood cells can cause partial obstruction of the airway, resulting in wheezing. The extent of lung involvement depends on the patient's immune response and the virulence of the infecting organism.


In the healthy adult, host mechanisms prevent disease much of the time. However, a number of mechanisms allow pathogens to gain entry into the lungs; these mechanisms include an altered level of consciousness due to stroke, seizure, anesthesia, alcohol abuse, intoxication, or the sleep state. Epiglottic closure may be compromised in these situations and allow normal oral flora to gain entry. Certain other conditions may predispose an individual to recurrent pneumonia, including compromised immune function, cystic fibrosis, esophageal abnormalities, bronchial obstruction, and bronchiectasis.

Proton pump inhibitors are powerful suppressants of gastric acid that are widely used (both over the counter and by prescription) to treat dyspepsia, gastroesophageal reflux, peptic ulcer, and gastritis. Studies have suggested that the widespread use of these agents may be contributing to the increase in both CAP and nosocomial pneumonia [19,20]. The suggested mechanism of this relationship is an increase in bacterial colonization of the upper gastrointestinal tract due to the suppression of acid. To date, there are no recommendations on withholding proton pump inhibitors from patients considered to be at high risk for development of pneumonia.



Gram-Positive Bacteria

S. pneumoniae is the leading cause of CAP in any adult age-group, with or without comorbid conditions [5,6,7,10]. Between 20% and 60% of all hospitalized pneumonia patients are infected with pneumococci [6]. Bacteremia caused by pneumococcal pneumonia is associated with a 20% mortality rate [21]. Those at risk for S. pneumoniae infection characteristically have some chronic condition, such as diabetes, COPD, asplenia, advanced age, cigarette smoking, congestive heart failure, dementia, alcoholism, or immunosuppression.

Patient history in those with S. pneumoniae infection may include an abrupt onset of high fever with shaking chills, productive cough with purulent sputum, and possibly pleuritic-type chest pains. Physical examination often reveals signs of consolidation (e.g., egophony, increased fremitus, dullness to percussion, rales, and rhonchi), and chest x-ray may show single or multiple lobar consolidation. Sputum analysis by Gram stain indicates gram-positive diplococci in pairs and short chains and large numbers of polymorphonuclear leukocytes [6].

S. aureus, although rarely a cause of CAP, should be considered, especially in patients with a primary influenza infection, in older adults, and in those with diabetes. An estimated 2% to 10% of acute CAPs are due to staphylococci [21]. Suppurative conditions, including empyema, lung abscess, and pneumothorax, are common complications. Seeding to distant sites, such as bones, joints, liver, endocardium, and the meninges, may also occur.

Group A streptococci rarely cause CAP but have been found in epidemics among close groups that live together, such as military units. Symptoms may be similar to those of S. pneumoniae. Gram stain reveals clumped spherical cocci, similar in appearance to a bunch of grapes [6].

Gram-Negative Bacteria

Although it is much less common than illness caused by gram-positive organisms, CAP may be the result of infection with gram-negative bacteria. H. influenzae, a possible etiologic agent of CAP, is a small, gram-negative rod with a polysaccharide capsule. There are six serotypes, of which type b is the most severe and invasive (causing meningitis and sepsis) [6]. Some strains of H. influenzae are nonencapsulated and therefore cannot be typed. These are also capable of causing disease, but usually the disease is noninvasive and therefore less severe. These non-typeable strains of H. influenzae are usually found in acute bronchitis; pneumonia caused by H. influenzae is generally caused by an encapsulated strain. Older adults and those with underlying chronic lung conditions are most susceptible to these bacteria [4,22]. The history usually includes an abrupt onset of fever, shaking chills, and cough with purulent sputum. The patient may describe pleuritic chest pain, and physical examination often reveals signs of consolidation. A bronchopneumonia pattern is seen on the chest x-ray.

Atypical CAP Syndromes

The first use of the term atypical pneumonia was in 1938 to describe a series of seven patients who had developed an unusual form of tracheobronchitis [21]. There had also been descriptions of outbreaks of pneumonia that behaved atypically in Europe in the 1920s. In general, these outbreaks were milder and had higher survival rates than the dominant strains of pneumonia. In the 20th century, the vast majority of atypical pneumonias were felt to be community acquired [21].

Atypical pneumonia syndromes largely refer to pneumonias caused by bacterial and nonbacterial organisms that do not share the expected characteristics of most bacteria [23]. M. pneumoniae is the most common cause of atypical pneumonia in those younger than 40 years of age; it disproportionately affects older children and young adults [24]. M. pneumoniae infections are extremely prevalent, and infections may be endemic in densely populated areas, such as schools, college dormitories, military barracks, and nursing homes [24]. Outbreaks often cluster in families, and close contacts of known infected patients show concordance rates as high as 50% [25]. Pneumonia due to M. pneumoniae usually results in mild disease, but occasionally can be life-threatening [24]. Infection due to M. pneumoniae should always be considered in the differential diagnosis of CAP, particularly when more than one household member is affected.

Atypical pneumonia syndrome is characterized by a prodrome of fever, headache, myalgia, and dry cough. These individuals usually appear less ill than those with typical bacterial pneumonia. However, symptoms may last up to 4 to 6 weeks and include a dry, hacking cough that may require a narcotic cough suppressant [21,24]. Because of the long incubation period, mycoplasmal infection may spread slowly among family members. It should be viewed as a systemic disease with a pulmonary component.

The physical examination usually reveals fine rales with no signs of lung consolidation. A cutaneous manifestation may be present in the form of maculopapular eruptions. Rarely, examination of the tympanic membranes shows evidence of bullous myringitis, which can be very painful. Chest x-ray reveals patchy alveolar densities or inhomogeneous segmental infiltrates. The white blood cell count may be normal or only slightly elevated. Full recovery is expected with no residual effects in a previously healthy individual. However, the disease can be severe in those with sickle cell anemia, older adults, and those with immunosuppression [21]. Treatment of M. pneumoniae infection requires administering an effective antibiotic. It is not sensitive to penicillin or other beta-lactam antibiotics, but it may be treated with macrolides, fluoroquinolones, or tetracyclines [21,24].

In younger patients, C. pneumoniae (TWAR strain) is the etiologic agent for a common atypical pneumonia syndrome. Outbreaks tend to occur in group living situations, such as military units and college dormitories [26]. Symptoms are similar to those described for mycoplasmal infection, although clinical presentation may also include laryngitis, a hoarse voice, and nonexudative pharyngitis [26]. Laryngitis is not present in any other atypical pneumonia syndrome. Chest x-ray may show patchy consolidation, interstitial infiltrates, or funnel-shaped lesions. The white blood cell count is usually normal.

Nonbacterial Pathogens

As noted, multiple viruses, including adenoviruses, respiratory syncytial virus (RSV), and parainfluenza virus, may also cause pneumonia [27]. Predilection for infection in children is the most common indicator of viral pneumonia. Cytomegalovirus and Pneumocystis jiroveci (a fungus) cause pneumonia in immunocompromised patients. Pneumonia caused by P. jiroveci, previously named Pneumocystis carinii, is considered an acquired immunodeficiency syndrome (AIDS)-defining opportunistic infection in the United States [28]. Infection with Hantavirus organisms may resemble a pneumonia syndrome, and this may be an issue in endemic areas such as the Southwestern United States. Hantavirus infection presents with fever, myalgia, and respiratory distress resembling acute respiratory distress syndrome [6].

RSV is another important potential cause of pneumonia in very young children and older adults [29]. Studies in which RSV was isolated by viral culture have demonstrated that it is common, occurring in 3% to 10% of older adults with pneumonia [30]. The incidence is similar in high-risk and healthy seniors, totaling about twice the incidence of influenza A [30]. RSV is also a common cause of infection in infants and young children, and it is estimated that most children have had RSV by 2 years of age [31]. It is leading cause of pneumonia in infants younger than 1 year of age, with 25% to 40% of those infected developing signs of pneumonia or bronchiolitis [29]. Premature birth, very young age, compromised immune system, and impaired lung or heart function are all risk factors for RSV-related pneumonia in infants.

Within the last decade, three newer pathogens have been added to the list of etiologic agents for atypical CAP: the coronavirus (CoV), which is responsible for severe acute respiratory syndrome (SARS); human metapneumovirus (hMPV); and community-acquired MRSA (CA-MRSA). The SARS-CoV was not documented in humans until 2002, when it was hypothesized that a previously unknown animal CoV may have mutated and infected humans [30]. There is no specific treatment for SARS, and management is primarily supportive. SARS-CoV is highly contagious, so aggressive infection control measures are necessary to prevent spread of the disease [30].

The paramyxovirus hMPV was first isolated in 2001 in children hospitalized with acute infections. Since then, hMPV has been reported in all age-groups and with varying stages of disease, from asymptomatic carrier states to severe bronchitis and pneumonia. Like SARS-CoV, there is no specific treatment for hMPV [30].

CA-MRSA is a combination of well-known healthcare-associated MRSA strains and newer isolates with distinctive genotypes. CA-MRSA is a virulent and resistant pathogen and causes outbreaks of serious infections, including skin and soft tissue infections and necrotizing pneumonia [30].


Gram-Positive Bacteria

While the majority of healthcare-associated pneumonias are caused by gram-negative bacteria, an estimated 20% to 30% are linked to infection with a gram-positive organism [32]. The most common gram-positive bacterium causing healthcare-associated pneumonia is S. aureus. Use of intravascular catheters and nasal carriage of S. aureus are the major risk factors for the development of gram-positive bacterial pneumonia in the healthcare setting [32,33].

Traditionally, S. aureus pneumonia has been considered a secondary infection following upper respiratory influenza infection [34]. However, it is now recognized as a significant cause of healthcare-associated pneumonia in the absence of influenza or other primary infection. Initially, primary staphylococcal pneumonia presents with fever. Later symptoms include respiratory distress, including tachypnea, retractions, and cyanosis, which may become rapidly severe [35]. Patients may also have gastrointestinal symptoms. Treatment depends upon the susceptibility of the organism.

Gram-Negative Bacteria

Aerobic gram-negative bacilli rarely colonize the upper airway in healthy individuals but are often found in people with an underlying disease, such as alcoholism, and in those who reside in healthcare facilities or nursing homes. Aspiration of the organisms is thought to be the mode of infection [32]. Pseudomonas spp., K. pneumoniae, and Escherichia coli may also become pulmonary pathogens. Therefore, a history of recent hospitalization or nursing home residency should heighten suspicion for a gram-negative pathogenesis. Polymicrobial infection is seen in up to 50% of cases of healthcare-associated pneumonia and is more common in older adults. Increased colonization of gram-negative bacilli of the upper airway is related to recent antimicrobial use, decreased activity, diabetes, and alcohol use [32].

M. catarrhalis is a beta-lactamase-producing, gram-negative aerobic diplococcus that is commonly found in individuals with COPD [6,7]. In patients with COPD, it is often the only organism isolated from the lower respiratory tract. Other chronic conditions, such as alcoholism, steroid use, diabetes, and malignancy, increase the risk of M. catarrhalis infection [7]. The highest incidence of this infection tends to be in the winter months [6].

Antibiotic therapy for healthcare-associated pneumonia is based on the patient's risk factors for infection with a multidrug-resistant organism, such as MRSA, P. aeruginosa, K. pneumoniae, or Acinetobacter. The American Thoracic Society lists the following risk factors for multidrug-resistant pneumonia in patients presenting with healthcare-associated, hospital-acquired, or ventilator-associated pneumonia [4]:

  • Antimicrobial therapy in the last 90 days

  • Current hospitalization of 5 days or more

  • High frequency of antibiotic resistance in the community of residence or the hospital unit of residence

  • Hospitalization for 2 days or more in the preceding 90 days

  • Residence in a nursing home

  • Home infusion therapy

  • Chronic dialysis within 30 days

  • Family member with multidrug-resistant infection

  • Immunosuppression

Hospital-Acquired Pneumonia

In 2011, an estimated 157,500 cases of hospital-acquired pneumonia were reported in U.S. hospitals [36]. As noted, hospital-acquired pneumonia is most frequently caused by bacteria, although some may be caused by viral pathogens such as influenza, parainfluenza, adenoviruses, and RSV. Influenza A is likely the leading cause of viral hospital-acquired pneumonia [4].

Hospital-acquired pneumonia and surgical-site infection are the two most common nosocomial infections in the United States. Hospital-acquired pneumonia is associated with mortality rates of up to 33% [37]. In the United States, patients with a hospital-acquired pneumonia have their average hospital stay lengthened by approximately 7 to 9 days, with an increase in cost of up to $40,000 [4].

Atypical Healthcare-Associated Pneumonias

Atypical pneumonias have historically been attributed to pathogens in the community setting. They were rarely thought to be a cause of healthcare-associated or hospital-acquired pneumonia, due to the dominance of a few prevalent strains and the lack of a reservoir (such as soil or animal vectors). However, it has become increasingly clear that atypical pneumonias can and do develop in the healthcare setting. One particularly common pathogen is L. pneumophila.


Legionella was first isolated from the blood of a laboratory worker who contracted the disease in 1947. While unable to identify the organism at that time, researchers saved samples, which later proved to be L. bozemanii [6]. There are 48 identified species of Legionella, although L. pneumophila is the primary pulmonary pathogen [18].

As discussed, the first recorded outbreak of legionellosis occurred in 1976 at an annual convention of the American Legion in Philadelphia [8]. A total of 182 of the delegates (many of whom were elderly) became ill, and 146 were hospitalized. Due to the conference having ended prior to the development of significant symptoms in many patients, hospitals all over the United States admitted one or more of the patients who had attended the convention. The mortality rate associated with this outbreak (16%) remains one of the highest for any legionellosis outbreak in history [8]. Despite an outpouring of resources, it took 6 months to isolate the organism, later named L. pneumophila. The pneumonia caused by the organism is commonly known as Legionnaires' disease [21].

Legionella spp. account for an estimated 8,000 to 18,000 cases of hospitalization for pneumonia in the United States each year, making it a leading atypical pneumonia [18,38]. The wide variability is due to the cluster nature of the disease in settings such as nursing homes.

L. pneumophila is a gram-negative bacillus and is considered an atypical organism because it does not respond to the beta-lactam antibiotics as other gram-negative organisms do. Suspicion for infection with Legionella organisms should be high in older adults and in those with chronic underlying disease, as these individuals have the highest mortality rates. Legionella bacteria grow in fresh water and are able to colonize complex water systems, including [39]:

  • Cooling towers

  • Humidifiers

  • Respiratory therapy equipment

  • Whirlpool spas

  • Evaporative condensers

  • Potable water distribution systems (e.g., showers, faucets)

Symptoms of infection include dry cough, fever of 38.3°C–38.8°C (101°F–102°F), altered mental status, relative bradycardia, headache, and gastrointestinal symptoms, including diarrhea. Chest x-ray reveals rapid progression of asymmetric infiltrates without signs of consolidation. Serum titer levels for Legionella organisms can be obtained but are often negative early in the disease. Confirmation of legionellosis requires a 4-fold or greater rise in antibody titer in paired acute and convalescent indirect fluorescent antibody tests obtained 4 to 8 weeks apart. A single elevated titer greater than 1:256 does not confirm a diagnosis; titers of 1:256 or more are found in 1% to 16% of healthy adults and children [39]. Urine antigen assay tests for exposure are widely available and are the preferred initial tests for Legionnaires' disease [39]. Antigen can be found in the urine of infected individuals up to 3 months postinfection, making it helpful in epidemiology studies [18].

The treatment recommendation for legionellosis is a fluoroquinolone, preferably levofloxacin [3]. Although previous recommendations for treatment included macrolide antibiotics, fluoroquinolones have proven superiority.

Prevention of Legionella transmission should be a major public health concern. The Centers for Disease Control and Prevention (CDC) has established guidelines for eradication of Legionella from water supply systems that include either superheating or hyperchlorinating the system [18,40].


Aspiration pneumonia is caused by the inhalation of oropharyngeal secretions colonized by pathogenic bacteria. If gastric contents are aspirated rather than infectious fluids, the resulting illness is referred to as chemical pneumonia. Chemical pneumonia is noninfectious and will not be discussed in this course.

The epidemiology of aspiration pneumonia is difficult to document, as there are no specific markers. Several studies have suggested that aspiration pneumonia may account for as many as 5% to 15% of CAPs [5]. Although the exact number of healthcare-associated aspiration pneumonia cases is unknown, steps to prevent the disease are noted in recommendations to decrease the number of nosocomial infections overall. Aspiration pneumonia is a considerable burden for nursing home patients, accounting for up to 18% of all nursing home-associated pneumonias [5].

The clinical presentation of aspiration pneumonia is similar to that described for CAP, with fever, chills, productive cough, and possibly pleuritic chest pain. If aspiration pneumonia develops in a healthcare setting, the onset may be more abrupt. Diagnosis is made with the presence of an infiltrate (visualized by radiograph) and predisposing factors for aspiration, including dysphagia, altered level of consciousness (e.g., dementia, coma, stroke, overdose), certain esophageal conditions, or use of a nasogastric or endotracheal tube [41].


Pneumonia is defined as lower respiratory tract infection that is associated with symptoms of acute onset with or without new infiltrate on chest radiographs. It is further classified according to the causative pathogen and the origin of the infection (i.e., community or healthcare facility). Clinical features will vary according to the etiology, but several commonalities exist.


The clinical presentation of pneumonia includes a history of fever, malaise, and cough with or without sputum production. The patient may also complain of hemoptysis, dyspnea, and pleuritic chest symptoms. Assessment should focus on identifying symptoms of bacterial, viral, and atypical pneumonia syndromes. Chest auscultation may reveal rales that do not clear with a cough, which may be found in both bacterial and atypical pneumonia. Consolidation, including dullness to percussion, bronchial breath sounds, and egophony (E-to-A changes), is found more commonly in the bacterial pneumonia syndromes [42]. Chest radiographs are highly variable and may be normal in the early course of the disease. However, chest x-rays of patients with viral and mycoplasmal pneumonia may show large infiltrates with minimum outward symptoms. A prodrome of headache and sore throat is often associated with atypical pneumonia. Patients between 18 and 44 years of age are almost twice as likely to complain of pleuritic chest pain and have fever as those who are older than 75 years of age. Some patients, including the elderly, may show none of the classic signs of pneumonia but may have atypical complaints, such as fatigue, lethargy, decreased appetite, increased falls, and mental status changes, such as confusion, stupor, or coma [42]. In addition, older adults are more likely to be seen initially with tachypnea but less likely to have a cough or fever.

It is important to remember that although influenza and other viral syndromes causing upper and lower respiratory symptoms do not respond to antibiotics, they may respond to antiviral medications. Furthermore, bacterial pneumonia may easily occur after a primary viral infection. While a patient may present to the primary care provider with an obvious acute viral syndrome, if he or she then presents 7 to 10 days later with a worsening of symptoms, it is likely that a bacterial infection has superimposed on a viral infection. The causative pathogen may be indicated by the patient's signs and symptoms and the clinical course of the disease.


The results of chest x-ray are most valuable when considered in the context of the history and physical examination. Both the IDSA and the American Thoracic Society recommend a chest x-ray for all patients diagnosed with pneumonia, both to establish the diagnosis and to rule out complications, although this may not always be feasible [42]. Posteroanterior and lateral chest x-rays confirm pneumonia when new infiltrates are found on the films. Characteristic bacterial patterns evident on the chest x-ray include lobar consolidation, cavitation, and large pleural effusions. However, a negative chest x-ray does not exclude the diagnosis of pneumonia; dehydration and neutropenia may result in false-negative findings [42]. Comparison of current and older radiographs is always important to assess for changes.


Analysis of sputum can be helpful in identifying the etiologic agent in pneumonia; however, guidelines do not recommend routine sputum samples be obtained from outpatients diagnosed with CAP [42]. If utilized, culture and Gram stain are excellent methods of identifying the pathologic agent. A good sputum sample comes from the bronchial tree; it is not the same as saliva from the mouth. Sputum produced on awakening in the morning is typically a good sample because of the strong reflex to cough when rising to an upright position. Sputum that contains less than 10 squamous epithelial cells and more than 25 neutrophils is considered an adequate sample. The patient is encouraged to rinse the mouth with water several times before trying to produce a sample. Inhalation of a warmed 3% to 10% saline solution may help the patient provide an adequate sample.


Multiple serologic and antigen studies are available to help identify the pathogen(s) responsible for a pneumonia. For example, the rapid BinaxNOW S. pneumoniae urinary antigen test may be used for the diagnosis of pneumococcal infection in hospitalized patients [43]. Results are available in 15 minutes, and the test has a sensitivity and specificity of 86% and 94%, respectively [43]. These tests are not routinely used in the outpatient setting.

Diagnostic recommendations for CAP patients requiring hospital admission include assessment of gas exchange either by telemetry or arterial sampling, complete blood count with differential, blood chemistry, liver function tests, and two sets of blood cultures. There is no evidence of benefit of routine bronchoscopy [42].


Multiple organisms must be considered in the differential diagnosis of pneumonia, as should syndromes that can mimic symptoms of the disease. These include pulmonary emboli, congestive heart failure, pulmonary tumors, and some inflammatory lung diseases.

Aspiration pneumonia may often be confused with, or be accompanied by, aspiration pneumonitis. Viral pneumonia may be hard to differentiate from bacterial pneumonia, but empiric antibiotic therapy should not be withheld from adult patients with disease of unknown etiology. A diagnosis of M. tuberculosis should be considered in patients with a history of hemoptysis, weight loss, immunocompromise, and/or exposure to active tuberculosis. A negative purified protein derivative tuberculosis test may be present in up to 25% of all patients with active tuberculosis and should not be considered proof that the patient does not have tuberculosis [42]. If active tuberculosis is suspected, the patient should be placed in isolation in a negative pressure room and consultation with a pulmonary or infectious disease specialist should be obtained.




Antibacterial agents are among the most commonly prescribed drugs worldwide, yet the advent of these drugs is a fairly recent phenomenon. Prior to the development of modern antibiotics, the treatment of pneumonia was difficult. The first treatment that showed a reduction in morbidity and mortality in the treatment of pneumococcal disease was actually the administration of an antipneumococcal antiserum obtained by injecting horses with pneumococcus. Use of antiserum resulted in a reduction in mortality from 25% to 7.5% [28]. The use of antiserum to treat pneumococcal pneumonia was a major public health initiative in the 1930s and heralded a change from the primary care practitioner as a solitary entity to the practitioner as a member of a larger, centralized healthcare team [28]. This revolution was short lived however, as the advent of sulfonamides had begun in the early 1900s. Sulfapyridine was the first well-tolerated, soluble sulfonamide and was in wide use by 1939 [30].

In 1942, the drug that would change the face of infectious disease treatment, penicillin, first became commercially available. With activity against pneumococcal disease, syphilis, and staphylococci, it was widely regarded as a miracle drug. Between 1900 and 1951, pneumonia deaths dropped from 200 per 100,000 to only 31 per 100,000 [30]. Research (both historical comparisons and drug-to-drug studies) shows that the mortality for patients receiving no treatment for pneumococcal pneumonia was 30.5%; for patients treated with antiserum treatment, the mortality rate decreased to 16.9%; for patients treated with sulfonamides, the rate declined to 12.3%; and finally in patients receiving penicillin or tetracycline, the rate dropped to 5.1% [30]. Then, as now, mortality increased with age. Since the advent of penicillin, studies of the effect of antibiotics on mortality in human subjects with pneumonia no longer contain a "no treatment" or placebo arm, as this would be highly unethical. Instead, studies are now based on the "inferiority" standard, or comparing the treatment outcome of a known drug with the outcome of a new, unknown drug.

Mechanisms of Action

Antibiotics are drugs that have a unique mechanism of action against targets not present in mammalian cells [6]. This limits toxicity to the host (patient) while allowing maximal efficacy against the target bacteria. The term bactericidal refers to drugs that are able to kill invading bacteria; bacteriostatic refers to drugs that are able to inhibit growth but not eradicate the offending organism. Bacteriostatic activity is sufficient for recovery from many bacterial infections in immunocompetent hosts, but bactericidal activity may be necessary for patients with immunosuppression or particularly virulent infections [6]. Different classes of antibiotics have different mechanisms of action, as discussed in the following sections.

Inhibition of Cell Wall Synthesis

Mammalian cells do not have a cell wall, but in bacteria, the cell wall protects the cell from osmotic rupture (the result of movement of liquid into a cell based on pressure). Most bacteria are hyperosmolar and will readily rupture without the presence of an intact cell wall. Cell wall rigidity and resistance to osmotic rupture is conferred by peptidoglycan, a covalently linked sacculus that surrounds the bacteria [6]. Antibiotics that interfere with the synthesis, export, assembly, or cross-linking of peptidoglycan can lead to inhibition of cell growth and cell death.

Antibiotics that inhibit cell wall synthesis include beta-lactams (penicillins, carbapenems, monobactams, and cephalosporins), glycopeptides (vancomycin and telavancin), and bacitracin. Beta-lactams are characterized by a four-membered lactam ring and inhibit cell wall cross-linking. Vancomycin and telavancin interfere with the addition of new wall subunits, and bacitracin prevents the addition of cell wall subunits by inhibiting recycling of the membrane lipid carrier [6,44]. Almost all antibiotics that inhibit cell wall synthesis are in fact bactericidal.

Inhibition of Protein Synthesis

Antibiotics may also interfere with protein synthesis by interacting with the bacterial ribosome. Bacterial ribosomes and mammalian ribosomes are different enough that antibiotics with this action are able to be selective for bacteria.

Antibiotics that utilize this mechanism include the aminoglycosides (gentamicin, kanamycin, tobramycin, streptomycin, neomycin, and amikacin). These agents bind irreversibly to the 30S subunit of the bacterial ribosome and block initiation of protein synthesis. Uptake of aminoglycosides is an aerobic, energy-dependent process. Therefore, aminoglycoside activity is extremely reduced in anaerobic environments. Aminoglycosides are generally bactericidal [6].

Macrolide antibiotics also inhibit protein synthesis. This class of antibiotics includes erythromycin, clarithromycin, and azithromycin. Ketolide antibiotics (telithromycin) are closely related to the macrolides and have the same mechanism of action. These antibiotics bind to the 50S portion of the bacterial ribosome [6].

Inhibition of protein synthesis is also found in tetracyclines, which react irreversibly with the 30S ribosomal subunit. Linezolid, the first of its kind in the oxazolidinone antibiotic class, acts by binding to the 50S ribosomal subunit [6].

Mupirocin, a topical antibiotic useful in the treatment of MRSA infections and asymptomatic colonization of the nares, has a unique mechanism of action. This agent inhibits protein synthesis by binding to isoleucyl transfer-RNA synthetase [6].

Inhibition of Bacterial Metabolism

Antimetabolites are synthetic compounds that inhibit bacterial synthesis of folic acid. This category of antibiotics includes sulfonamides, which compete with para-aminobenzoic acid in the synthesis of folic acid, and trimethoprim, which inhibits a folic acid synthesis pathway.

Inhibition of Nucleic Acid Synthesis

The primary antibiotics with action against nucleic acid synthesis are the quinolones (ciprofloxacin, levofloxacin, gatifloxacin, and moxifloxacin). These drugs inhibit the activity of the A subunit of the bacterial enzyme DNA gyrase. Other drugs that inhibit nucleic acid synthesis include rifampin (primarily used in the treatment of M. tuberculosis), nitrofurantoin (causes DNA strand breakage and is primarily used in the treatment of urinary tract infections), and metronidazole.

Metronidazole causes DNA damage and is useful in the treatment of anaerobic bacteria and protozoal infections [45]. It is often prescribed topically for rosacea and can be used topically for vaginal infections. When used systemically, a disulfiram-type reaction may develop when taken with alcohol, and patients should be instructed to avoid alcohol while taking metronidazole [45].

Bacterial Resistance

Bacterial resistance to antibiotics can take two forms: intrinsic and acquired. Intrinsic resistance is present when bacteria are naturally resistant to an antibiotics mechanism of action. For example, gram-negative bacteria are intrinsically resistant to vancomycin. Of particular interest now is the development of bacterial resistance to antibiotics to which they were previously susceptible. This resistance is generally acquired either by the mutation of existing genes or by the acquisition of new genes (e.g., by exchange of plasmids among bacteria). Resistant bacteria tend to grow prolifically in the presence of antibiotics to which they are resistant, due to the elimination of nonresistant bacteria. Mechanisms of resistance include inactivation, overproduction of the antimicrobial's target, genetic alteration of the antimicrobial's target, decreased permeability in relation to the antimicrobial, and active elimination of the antimicrobial from the target cell.

Resistance to Beta-Lactam Antibiotics

The most common type of acquired resistance to beta-lactam antibiotics is via the development of beta lactamase, which destroys the beta-lactam antibiotic. Both gram-negative and gram-positive bacteria may produce beta lactamase. Certain advanced generation beta-lactam antibiotics, such as cefepime and ceftaroline, are stable in the presence of plasmid mediated beta lactamase [45]. However, other types of acquired beta lactamase production may be resistant to all beta-lactam antibiotics.

Resistance to Vancomycin

Vancomycin resistance in enterococci was first identified in 1988 [46]. Since then, vancomycin-resistant enterococci (VRE) have become widely spread and now rank as one of the leading nosocomial infections. Enterococci develop vancomycin resistance by the transfer of plasmids from cell to cell and from transposons that can jump from plasmids to chromosomes. Resistance leads to the elimination of the vancomycin binding site on resistant bacteria. Originally, only enterococci were able to demonstrate this acquired resistance, but beginning in the 2000s, S. aureus highly resistant to vancomycin was isolated in the United States [46]. Genetic testing demonstrated that the gene responsible for resistant S. aureus was from VRE. There have also been cases of vancomycin resistant S. aureus with other forms of resistance, including cell wall thickening. Isolates of S. epidermis have also been found to have vancomycin resistance due to cell wall thickening [46].

Resistance to Aminoglycosides

Aminoglycoside resistance is usually a result of inactivation of the antimicrobial, usually mediated by acquired plasmids. This results in diminished binding to the ribosomal target. This resistance can be found in both gram-negative and gram-positive bacteria.

Resistance to Macrolides

Resistance to macrolide antibiotics is generally due to the production of an enzyme that interferes with the binding of macrolides to their target. Macrolides are generally only effective against gram-positive bacteria, so this resistance is only found in gram-positive bacteria. Resistance to macrolides is considered a plasmid-acquired resistance.

Resistance to Tetracyclines

Tetracycline resistance is usually via a very interesting plasma-mediated resistance. The cell acquires the ability to develop a pump that eliminates the antimicrobial from inside the cell. This resistance is found in gram-negative bacteria, although gram-positive bacteria may also develop tetracycline resistance, either due to the ability of the bacteria to eliminate tetracycline or diminish its ability to bind to the cell.

Resistance to Sulfonamide and Trimethoprim

Sulfonamide and trimethoprim resistance is generally a plasmid-mediated resistance. Bacteria evolve to eliminate the target site of action of the drugs.

Resistance to Quinolones

Quinolone resistance is seen in Staphylococcus spp., Pseudomonas spp., S. pneumoniae, and E. coli. A DNA mutation prevents the antimicrobial from exerting its antienzyme activity. In addition, gram-negative bacteria may develop resistance by expelling the antimicrobial from the cytoplasm or decreasing cell wall permeability.

Resistance to Linezolid

Despite the fact that linezolid is a newer antimicrobial, clinical resistance has been found. E. faecium and E. faecalis have developed resistance by mutation of the binding site.

Multidrug-Resistant Organism Development

While resistance of bacteria to one antibiotic or class of antibiotics is of clinical importance and affects how clinicians treat patients, the development of resistance to multiple drugs is a major public health concern. MRSA, vancomycin-resistant MRSA, and multidrug-resistant and extremely drug-resistant M. tuberculosis are the subject of much investigation. Strains of bacteria resistant to all available antibiotics have been identified and threaten to allow pneumonia to once again be a major source of morbidity and mortality.

Multidrug resistance can be the result of sequential mutations, acquisition of multiple unrelated genes, or acquisition of a single gene that confers resistance to multiple drugs. Sequential acquisition of genes tends to occur in environments with high levels of antimicrobials (e.g., in an intensive care setting), but acquisition of a single mutation that confers multiple resistance may occur in any setting. Bacteria with multidrug resistance can include enterococci, staphylococci, Salmonella, gonococci, and pneumococci. Gram-negative bacteria often acquire multidrug resistance via genes that allow for the elimination of antimicrobials from the cell as well as genes that encode for the outer membranes of cells.


Resistance patterns to all antibiotics are an increasing problem, more widespread now than at any other time in medical history. Careful, prudent use of antibiotics is absolutely necessary to curb this growing problem. The routine practice of trying to cover for all pathogens, especially gram-negative organisms, should be avoided; this only leads to increased resistance patterns. Initiation of antibiotic treatment, particularly in patients with CAP, is empirically determined because the history and physical examination will not determine the specific pathogen responsible for the disease [12,47,48,49]. Even with sputum culture, Gram stain, and chest x-ray, providers can only accurately identify the causative organism 40% to 70% of the time [3,4]. Therefore, the patient's age, location (e.g., community dwelling, healthcare setting), immunocompetency, and underlying chronic conditions will guide treatment decisions. Patterns of resistance in the community and knowledge of the most likely pathogens must also be considered when selecting an empiric antimicrobial therapy.

The choice of antibiotic therapy depends on careful consideration of the cost, the consequences of failing to respond to initial outpatient treatment, and the need for hospitalization. Additional concerns include the likelihood of adherence to the treatment regimen, the existence of a supportive home environment, access to emergency care if needed, the presence of an involved individual to identify significant changes in this illness should they occur, and the opportunity for follow-up in 24 to 48 hours.

Recommendations for initial empiric antimicrobial therapy in the outpatient setting vary [5,6]. Since the first publication of these recommendations in 1993, there has been a shift in focus from age-groups and comorbid conditions as the basis for drug selection to the most likely pathogens combined with modifying factors and/or co-existing cardiopulmonary disease (Table 2 and Table 3). Patients are categorized according to location and risk factors for complicated diseases. Group I includes outpatients without cardiopulmonary disease or modifying factors. Modifying factors include risk factors for infection with drug-resistant pneumococci, gram-negative infection (including nursing home residence), and infection with P. aeruginosa; human immunodeficiency virus (HIV) infection is also a factor [6]. Group II includes outpatients with cardiopulmonary disease (e.g., congestive heart failure or COPD) and/or other modifying factors (e.g., risk factors for drug-resistant S. pneumoniae or gram-negative bacteria). Group III consists of inpatients not in the intensive care unit (ICU), while group IV includes inpatients admitted to the ICU [6].


Penicillin-resistant and drug-resistant pneumococci
Age older than 65 years
Beta-lactam therapy within the past three months
Immunosuppressive illness (including therapy with corticosteroids)
Multiple medical comorbidities
Exposure to a child in a day care center
Enteric gram-negative organisms
Residence in a nursing home
Underlying cardiopulmonary disease
Pseudomonas aeruginosa infection
Structural lung disease (bronchiectasis)
Corticosteroid therapy (
Recent antibiotic therapy, especially broad-spectrum antibiotic therapy for more than seven days in the past month


Group I: Outpatients, no cardiopulmonary disease, no modifying factorsa
Streptococcus pneumoniae
Mycoplasma pneumoniae
Chlamydia pneumoniae (alone or as mixed infection)
Haemophilus influenzae
Respiratory viruses
Miscellaneous (Legionella spp., Mycobacterium tuberculosis, endemic fungi)
Macrolide or doxycycline
Group II: Outpatients with cardiopulmonary disease and/or other modifying factorsa
S. pneumoniae (including drug-resistant S. pneumoniae [DRSP])
M. pneumoniae
C. pneumoniae
Mixed infection (bacteria plus atypical pathogen or virus)
H. influenzae
Enteric gram-negatives
Respiratory viruses
Miscellaneous (Moraxella catarrhalis, Legionella spp., aspiration [anaerobes], M. tuberculosis, endemic fungi)
Beta-lactam (oral cefpodoxime, cefuroxime, high-dose amoxicillinb, amoxicillin-clavulanate; or parenteral ceftriaxone followed by oral cefpodoxime)
macrolide or doxycycline
respiratory fluoroquinolone
Group III: Inpatients not in ICUa
Cardiopulmonary disease and/or modifying factors (including being from a nursing home)
S. pneumoniae (including DRSP)
H. influenzae
M. pneumoniae
C. pneumoniae
Mixed infection (bacteria plus atypical pathogen)
Enteric gram-negatives
Aspiration (anaerobes)
Legionella spp.
Miscellaneous (M. tuberculosis, endemic fungi, Pneumocystis carinii)
Beta-lactamc (cefotaxime, ceftriaxone, ampicillin-sulbactam, high-dose ampicillin)
macrolide or doxycyclined
respiratory fluoroquinolone alone
No cardiopulmonary disease, no modifying factors
S. pneumoniae
H. influenzae
M. pneumoniae
C. pneumoniae
Mixed infection (bacteria plus atypical pathogen)
Legionella spp.
Miscellaneous (M. tuberculosis, endemic fungi, Pneumocystis jiroveci)
IV azithromycin alone
If macrolide allergic or intolerant: Doxycycline and a beta-lactam
monotherapy with an antipneumococcal fluoroquinolone
Group IV: ICU-admitted patientsa
No risk factors for Pseudomonas aeruginosa or multidrug-resistant pathogens
S. pneumoniae
Legionella spp.
H. influenzae
Enteric gram-negative bacilli
Staphylococcus aureus (methicillin sensitive)
M. pneumoniae
Respiratory viruses
Miscellaneous (C. pneumoniae, M. tuberculosis, endemic fungi)
levofloxacin, moxifloxacin, or ciprofloxacin
At risk for multidrug-resistant pathogens in patients with hospital-acquired pneumonia, ventilator-associated pneumonia, healthcare-associated pneumonia, or late-onset disease
All of the above pathogens plus
P. aeruginosa
Klebsiella pneumoniae
Acinetobacter spp.
Methicillin-resistant S. aureus (MRSA)
Legionella pneumophila
Antipseudomonal cephalosporin (cefepime, ceftazidime)
antipseudomonal carbapenem (imipenem or meropenem)
beta-lactam/beta-lactamase inhibitor (piperacillin/tazobactam)
antipseudomonal fluoroquinolone (ciprofloxacin or levofloxacin)
aminoglycoside (amikacin, gentamicin, or tobramycin)
linezolid or vancomycin
aExcludes patients at risk for HIV.
bHigh-dose amoxicillin is 1 g every 8 hours; if a macrolide is used, erythromycin does not provide coverage of H. influenzae, and thus when amoxicillin is used, the addition of doxycycline or of an advanced-generation macrolide is required to provide adequate coverage of H. influenzae.
cAntipseudomonal agents such as cefepime, piperacillin-tazobactam, imipenem, and meropenem are generally active against DRSP, but are not recommended for routine use in those in this population without risk factors for P. aeruginosa.
dUse of doxycycline or an advanced-generation macrolide (azithromycin or clarithromycin) will provide adequate coverage if the selected beta-lactam is susceptible to bacterial beta-lactamases.

Monotherapy generally is adequate treatment for outpatients with pneumonia without comorbid illness or modifying factors (group I) [6]. The most common pathogens in this group are S. pneumoniae, M. pneumoniae, respiratory viruses, C. pneumoniae, and H. influenzae. Other pathogens, including Legionella spp., M. tuberculosis, and endemic fungi, cause pneumonia to a lesser extent. The American Thoracic Society and the IDSA recommend a macrolide (azithromycin, clarithromycin, or erythromycin) for the treatment of this patient group, with doxycycline a possible alternative [6]. Clinicians should be aware of regional patterns of resistance that could make selection of a macrolide antibiotic inappropriate.

As noted, group II includes outpatients with cardiopulmonary diseases (congestive heart failure or COPD), liver or renal disease, asplenia, immunosuppression, recent use of antimicrobials (within the last 3 months), or risk factors for drug-resistant S. pneumoniae, which include an age older than 65 years and nursing home residence [6]. The pathogens are slightly different than those noted for group I, but pneumococci remain the most likely cause of pneumonia for this group, especially pneumococci that are resistant to penicillin. Other organisms include E. coli, Klebsiella spp., and P. aeruginosa. Aspiration with anaerobes should be considered if there is poor dentition, neurologic illness, or impaired consciousness. Recommended initial therapy includes beta-lactam drugs (penicillins and cephalosporins), with the addition of a macrolide or doxycycline; or monotherapy with an antipneumococcal fluoroquinolone (levofloxacin, moxifloxacin, or gatifloxacin). If local macrolide-resistant S. pneumoniae is common (>25%), consider use of non-macrolides for all patients [6].

In 2013, after the establishment of the current guidelines for the treatment of pneumonia, the U.S. Food and Drug Administration (FDA) approved telavancin, a glycopeptide like vancomycin, for the treatment of patients with hospital-acquired or ventilator-associated bacterial pneumonia caused by S. aureus [44]. Telavancin should only be used when other agents are not suitable.

The duration of therapy is usually 7 to 14 days, depending on the severity of the illness, presence of comorbidities, and resolution of the illness. The long half-life of azithromycin allows for a shorter duration of therapy, usually 3 to 5 days. Studies also support the use of higher (750 mg) daily dosing of levofloxacin for shorter treatment periods (5 days) [4]. In the immunocompromised patient, 50% additional time is generally needed for antibiotic therapy (10 to 21 days). Treatment of suspected mycoplasmal or chlamydial pneumonia should continue for 10 to 14 days. Infection with Legionella organisms, which takes the longest to resolve of all the CAPs, requires 14 or more days of antibiotic therapy [4,5,6,10].

Several newer antibiotics are also available for treating CAP. Appropriate treatment for CA-MRSA pneumonia includes vancomycin, linezolid, and possibly trimethoprim-sulfamethoxazole (TMP-SMX) and clindamycin [3,45]. It has yet to be determined if the addition of rifampin improves outcomes. Linezolid, the first of a new class of antibiotics called the oxazolidinones, is active against many gram-positive pathogens, including CA-MRSA, anaerobes, VRE, and penicillin-resistant S. pneumoniae. The main concern with CA-MRSA is the necrotizing aspect of the infection, and unfortunately, many treatment options have not yet been shown to decrease toxin production. Therefore, linezolid may be the best choice [30].

Older adults and those with co-existing illness tend to experience more virulent pneumonia, have longer healing times, and require more supportive treatment and closer follow-up monitoring, especially with delayed resolution of the disease [3]. Younger pneumonia patients without comorbid disease usually respond more quickly and have fewer complications. With the increased prevalence of HIV/AIDS and immunosuppressive therapies, the possibility of compromised immune function must be considered when there is delayed resolution of pneumonia or when a young individual seems to be more ill than would be expected. As discussed, P. jiroveci pneumonia is considered an AIDS-defining illness and may be suspected in at-risk patients whose illness does not respond to antibiotic treatment. Other pathogens more likely to cause disease in immunocompromised patients include S. pneumoniae, H. influenzae, cytomegalovirus, and M. tuberculosis.

In patients with underlying COPD, asthma, or other lung disease, adjunct medication strategies may be necessary. Consideration should be given to the patient's need for beta agonist therapy and to the possible initiation of steroids. Patients with asthma and audible wheezing should receive treatment with either inhaled or nebulized albuterol [3,4]. If the patient is stable and has moderate wheezing, inhaled corticosteroids may be considered. Inhaled steroids can be given via inhaler (flunisolide or budesonide) or via small-volume nebulizer (budesonide) [45].

Patients with COPD may benefit from combination therapy with albuterol and ipratropium, either via inhaler or small-volume nebulizer [3,4]. While not all COPD patients have steroid-responsive disease, if the patient has audible wheezing and bronchial constriction is present, steroid therapy should be considered. Again, the patient can be treated either with nebulized or inhaled steroids.

Patients requiring intravenous steroids, supplemental oxygen, intravenous antibiotics, or close monitoring should be referred for emergency evaluation [3]. Hospitalized patients may benefit from prophylactic subcutaneous low-molecular-weight heparin therapy for prevention of deep vein thrombosis [4]. Treatment can consist of low-molecular weight heparin, such as enoxaparin, either 40 mg daily or 30 mg every 12 hours [45].


With minimum diagnostic testing and empiric antibiotic treatment, most patients will improve and show resolution of pneumonia. In most cases, improvement is seen within 48 to 72 hours after initiation of antibiotics. Pneumonia that fails to resolve shows little clinical improvement after 4 weeks of therapy. Fever, cough, sputum production, and shortness of breath may still be present, and chest x-ray will fail to show improvement. If untreated, abscess, empyema, pulmonary vascular congestion, and/or pulmonary embolism may develop.

When there is poor response to therapy, there are several possible causes: the initial antibiotic choice was not correct, there was poor adherence to the oral antibiotic therapy, or the diagnosis of pneumonia was not accurate. Consideration should be given to less common causes of pneumonia and pneumonia-like symptoms, including opportunistic fungal infections, P. jiroveci infection, tuberculosis, bronchogenic carcinoma, Wegener's granulomatosis, bronchiolitis obliterans with organizing pneumonia, and congestive heart failure. A diagnostic bronchoscopy, computed tomography scan, and transthoracic needle aspiration and biopsy may be warranted to exclude these. If the diagnosis is still undetermined and there is no resolution, consultation with a pulmonologist is advised and an open lung biopsy may be considered.


Patients with delayed resolution of pneumonia or who are referred for inpatient treatment generally require consultation. Pneumonia is the leading cause of death resulting from an infectious agent, and it is imperative to recognize patients who are candidates for inpatient therapy. Certain clinical criteria observed in the patient warrant hospitalization [50]:

  • Severe abnormality in vital signs

    • Heart rate >125 beats per minute

    • Systolic blood pressure <90 mm Hg

    • Respiratory rate >30 breaths per minute

  • Altered mental status

  • Oxygen saturation by pulse oximetry less than 90% on room air

  • Suppurative pneumonia-related infection (e.g., empyema, septic arthritis, meningitis, endocarditis)

  • Severe electrolyte imbalance or metabolic abnormality not known to be chronic

    • Sodium <130 mEq/L

    • Hematocrit <30%

    • Absolute neutrophil count <1000/mm3 or white blood cell count <5000/mm3

    • Blood urea nitrogen (BUN) >50 mg/dL

    • Creatinine >2.5 mg/dL

  • Acute co-existent medical condition requiring hospital admission that is independent of pneumonia

  • Failure to respond to outpatient treatment within 48 to 72 hours

Although these findings are often indicative of a need for hospitalization, the healthcare provider's clinical judgment is often the best tool.


After a diagnosis of pneumonia has been made, patient education should include directions for use of the antibiotic and information on potential untoward effects of the drug. Follow-up instructions, depending on the clinical situation, may include 24-hour telephone contact or follow-up in the office after 24 to 48 hours. This will improve adherence to the prescribed therapy, provide an opportunity to address side effects of drug therapy, and allow progress to be monitored. The need for hospitalization should be assessed throughout the course of the illness. Education should also include instructions to drink plenty of fluids and to use an antipyretic to control fever and myalgias when needed. Use of cough suppressants should be avoided, as the cough reflex and sputum expectoration enhance removal of thick secretions. However, in the event of a constant, nonproductive cough, as found especially with mycoplasmal infection, a narcotic such as codeine at night may allow for more restorative sleep.

Provisions for patients with limited English language proficiency are required under federal law, and the U.S. Department of Health and Human Services and the Office of Civil Rights view a lack of adequate interpretation as discrimination, based on the Civil Rights Act of 1964 [51]. According to U.S. Census Bureau data from 2013, more than 60 million Americans speak a language other than English at home, with more than 25 million (8.6% of the population) reporting that they speak English less than "very well" [52]. Immigrant patients with chronic illness may feel unable to return to their home countries due to a lack of available medical care. Changes in healthcare law restricting federal funding of services to only legal residents may cause significant problems for certain facilities, with conflicts arising from providing life-saving care for patients who have no means of reimbursement and no medical services waiting for them in their home countries.


Vaccination is one of the most important health promotion interventions for patients at risk for developing pneumonia. In addition to vaccination, engaging in a healthier lifestyle can help prevent or lessen the impact of pneumonia. This includes engaging in regular physical activity, eating a healthy diet, practicing good hand hygiene, and avoiding smoke and contact with persons who have respiratory infections.


The 13-valent pneumococcal conjugate vaccine (PCV13) is recommended for all children younger than 59 months of age (minimum age: 2 months) [53]. PCV13 is also recommended for adults 19 years of age and older with certain medical conditions. In addition, children older than 24 months of age who are at high risk of pneumococcal disease and adults with risk factors may receive the 23-valent pneumococcal polysaccharide vaccine (PPSV23). In children, factors that increase the risk of developing pneumococcal disease include chronic heart or lung disease, diabetes, cerebrospinal fluid (CSF) leaks, cochlear implants, immunocompromising conditions (e.g., HIV), and congenital or acquired asplenia [54]. In adults, factors that support the administration of pneumococcal vaccine include diabetes, immunocompromising conditions, chronic lung disease, heart disease, chronic alcoholism, liver disease, and asplenia [55]. All adults older than 65 years of age should be encouraged to receive the PPSV23 vaccine. In addition, vaccination against influenza can reduce the incidence of secondary pneumonia in many patients. It is recommended that all individuals older than 6 months of age receive the influenza vaccine each year [54,55].


Good handwashing is difficult to practice, is rarely known or taught, and is one of the single most effective ways to prevent transmission of many diseases, including many pneumonias. Everyone knows to wash their hands before eating and after using the restroom. However, few do little more than remove obvious dirt. Good handwashing involves removing the skin oils where organisms can remain even when the hands look clean. A quick pass under the water faucet and fast dry with a towel removes visible dirt, but the oils and organisms remain.

To effectively remove the oils and organisms, the process should take at least 20 seconds—the amount of time it takes to sing "Twinkle, Twinkle Little Star." The hands should be soaped and rubbed vigorously for 15 seconds to create a good lather and to assure that all parts of each hand are scrubbed well. Then, the hands should be rinsed thoroughly and dried, preferably with a paper towel. The towel should be used to turn off the water and then properly thrown away. If there is no visible dirt or contamination, a waterless hand sanitizer with at least 60% alcohol can be used. However, nothing is as good as washing well with soap and water.

Some mistakenly believe that hot water must be used to kill the organisms. Water hot enough to kill organisms would be too hot to touch. Warm water mainly adds to comfort and hopefully encourages better washing technique. Careful attention to handwashing and cleansing may result in chapped skin, so lotions may be used to care for one's hands [56].

Preventing the Spread of Pneumonias

The eyes, nose, and mouth are entryways for bacteria and viruses. People tend to unconsciously touch their eyes, nose, and mouth when going about their activities. Because organisms are not visible and handwashing is often less than adequate, infection occurs. Though difficult, individuals trying to prevent illness should make a conscious effort to avoid touching their face [57].

Disposable paper tissues should be used to cover one's nose or mouth when coughing or sneezing. Hands will be contaminated with the offending virus or bacteria while covering. Ideally, the hands should be cleaned with soap and water or alcohol-based hand sanitizer after each cough or sneeze to prevent transfer of the organism to someone else. In reality, sneezes and coughs may often be covered with only a bare hand, which may not be washed immediately. Education of patients and children should include teaching them to cough and sneeze into their upper sleeve instead of into their hand. Covering a cough or sneeze is of primary importance however it is done [58]. Coughing, sneezing, or blowing nasal secretions into a cloth handkerchief results in maintaining a moist, viable culture that is then carried in the pocket or purse and can result in prolonged episodes of re-infection or transfer from cross-contamination.

If at all possible, individuals should avoid close contact with persons who are experiencing respiratory symptoms. Good handwashing should be done as soon as possible after contact with someone exhibiting symptoms of respiratory illness. Behaviors to help the immune system overcome organisms include getting enough rest, drinking 6 to 8 glasses of water a day, and eating fresh fruits and vegetables [59].


The CDC and the Healthcare Infection Control Practices Advisory Committee have developed guidelines for the prevention of healthcare-associated pneumonia caused by a variety of pathogens [40]. The following recommendations are reprinted from the publication Guidelines for Preventing Health-Care-Associated Pneumonia, 2003 [40].


Educate healthcare workers about the epidemiology of and infection-control procedures for preventing healthcare-associated bacterial pneumonia to ensure worker competency according to the worker's level of responsibility in the healthcare setting. Involve the workers in the implementation of interventions to prevent healthcare-associated pneumonia by using performance-improvement tools and techniques.


Conduct surveillance for bacterial pneumonia in ICU patients who are at high risk for healthcare-related bacterial pneumonia (e.g., patients with mechanically assisted ventilation or selected postoperative patients) to determine trends and help identify outbreaks and other potential infection-control problems. The use of the National Nosocomial Infection Surveillance (NNIS) system's surveillance definition of pneumonia is recommended, including data on the causative micro-organisms and their antimicrobial susceptibility patterns.


Sterilization or Disinfection and Maintenance of Equipment and Devices

Thoroughly clean all equipment and devices to be sterilized or disinfected. Whenever possible, use steam sterilization (by autoclaving) or high-level disinfection by wet heat pasteurization at >158°F (>70°C) for 30 minutes for reprocessing semicritical equipment or devices (i.e., items that come into direct or indirect contact with mucous membranes of the lower respiratory tract) that are not sensitive to heat and moisture for equipment or devices that are heat-or moisture-sensitive. After disinfection, proceed with appropriate rinsing, drying, and packaging, taking care not to contaminate the disinfected items in the process.

Preferentially use sterile water for rinsing reusable semicritical respiratory equipment and devices when rinsing is needed after they have been chemically disinfected. If this is not feasible, rinse the device with filtered water (i.e., water that has been through a 0.2 micron filter) or tap water, and then rinse with isopropyl alcohol and dry with forced air or in a drying cabinet.

Prevention of Person-to-Person Transmission of Bacteria: Standard Precautions

Decontaminate hands by washing them with either antimicrobial soap and water or with nonantimicrobial soap and water (if hands are visibly dirty or contaminated with proteinaceous material or are soiled with blood or body fluids) or by using an alcohol-based waterless antiseptic agent (e.g., hand rub) if hands are not visibly soiled after contact with mucous membranes, respiratory secretions, or objects contaminated with respiratory secretions, whether or not gloves are worn. Decontaminate hands before and after contact with a patient who has an endotracheal or tracheostomy tube in place, and before and after contact with any respiratory device that is used on the patient, whether or not gloves are worn.

Wear gloves for handling respiratory secretions or objects contaminated with respiratory secretions of any patient. Change gloves and decontaminate hands as described between contacts with different patients; after handling respiratory secretions or objects contaminated with secretions from one patient and before contact with another patient, object, or environmental surface; and between contacts with a contaminated body site and the respiratory tract of, or respiratory device on, the same patient. When soiling with respiratory secretions from a patient is anticipated, wear a gown and change it after soiling occurs and before providing care to another patient.


Vaccinate patients at high risk for severe pneumococcal infections. PPSV23 should be administered to all persons older than 65 years of age; persons 5 to 64 years of age who have chronic cardiovascular disease (e.g., congestive heart failure or cardiomyopathy), chronic pulmonary disease (e.g., COPD or emphysema, but not asthma), diabetes, alcoholism, chronic liver disease (e.g., cirrhosis), or CSF leaks; persons 5 to 64 years of age who have functional or anatomic asplenia; persons 5 to 64 years of age who are living in special environments or social settings; immunocompromised persons older than 5 years of age with HIV infection, leukemia, lymphoma, Hodgkin's disease, multiple myeloma, generalized malignancy, chronic renal failure, nephrotic syndrome, or other conditions associated with immunosuppression; and persons in long-term-care facilities [55]. Adults 19 years of age and older with immunocompromising conditions, asplenia, CSF leaks, or cochlear implants who have not been previously vaccinated should receive a single dose of PCV13 followed by a dose of PPSV23 at least 8 weeks later [55].

Administer PCV13 to all children younger than 59 months of age. For children 14 to 59 months of age who have received an age-appropriate series of 7-valent PCV, administer a single supplemental dose of PCV13.

In nursing homes and other long-term care facilities, establish a standing order program for the administration of PPSV23 to persons at high risk for acquiring severe pneumococcal infections, including pneumococcal pneumonia.

Precautions for Prevention of Aspiration

As soon as the clinical indications for their use are resolved, remove devices such as endotracheal, tracheostomy, and/or enteral tubes from patients. When feasible and not medically contraindicated, use noninvasive positive-pressure ventilation delivered continuously by face or nose mask instead of performing endotracheal intubation in patients who are in respiratory failure and are not needing immediate intubation (e.g., those who are in hypercapnic respiratory failure secondary to acute exacerbation of COPD or cardiogenic pulmonary edema). As much as possible, avoid repeat endotracheal intubation in patients who have received mechanically assisted ventilation.

In the absence of medical contraindication(s), elevate the head of the bed to an angle of 30 to 45 degrees for patients at high risk for aspiration (e.g., those receiving mechanically assisted ventilation and/or those with an enteral tube in place). Develop and implement a comprehensive oral-hygiene program, including oropharyngeal cleaning and decontamination with an antiseptic agent, for patients in acute-care settings or residents in long-term care facilities who are at high risk for healthcare-associated pneumonia.

Prevention of Postoperative Pneumonia

Instruct preoperative patients, especially those at high risk for contracting pneumonia, about taking deep breaths and ambulating as soon as medically indicated in the postoperative period. Patients at high risk for developing postoperative pneumonia include those who will have abdominal aortic aneurysm repair, thoracic surgery, or emergency surgery; those who will receive general anesthesia; those who are older than 60 years of age; those with totally dependent functional status; those who have had a weight loss greater than 10%; those using steroids for chronic conditions; those with recent history of alcohol use, COPD, or smoking during the preceding year; those with impaired sensorium, a history of cerebrovascular accident with residual neurologic deficit, or low (<8 mg/dL) or high (>22 mg/dL) BUN level; and those who will have received more than 4 units of blood before surgery.

Encourage all postoperative patients to take deep breaths, move about the bed, and ambulate, unless medically contraindicated. Use incentive spirometry on postoperative patients at high risk for pneumonia.


Intubation and mechanical ventilation are a leading cause of hospital-acquired pneumonia (and clearly a defining factor in the development of ventilator-associated pneumonia). These interventions increase the risk for developing hospital-acquired pneumonia up to 21-fold [4]. Alternatives to mechanical ventilation include noninvasive positive pressure ventilation via face mask [4]. Higher inspiratory pressure versus expiratory pressure, also referred to as bilevel positive airway pressure or BPAP, may be used for patients with acute exacerbation of COPD and/or patients with respiratory failure. Typical initial pressure regimens include inspiratory positive airway pressure (IPAP) of 10 cm water and an expiratory positive airway pressure of 5 cm water. Most BPAP machines have an oxygen blender, and oxygen settings can be determined by the patient's clinical condition. Rescue BPAP typically refers to having "back-up breaths" provided by the machine on an as-needed basis; if used in this capacity, the BPAP machine can be set to initiate a breath in the presence of apnea. Patient selection should exclude patients who require immediate intubation and patients who are unable or unwilling to cooperate with the procedure.

When intubation is required, steps may be taken to reduce the incidence of ventilator-associated pneumonia, although studies showing benefit from interventions are limited. Specially designed endotracheal tubes that allow for continuous suctioning of subglottic secretions may be useful [4]. Also, close attention to the prevention of ventilator circuit colonization (especially in the condensate in the tubing circuit) is important, although studies comparing the frequency of tubing circuit changes have failed to show a decrease in ventilator-associated pneumonia [4]. Other recommendations to address modifiable risk factors for ventilator-associated pneumonia include [4]:

  • Infection control measures, staff education, and attention to basic prevention of nosocomial infection via handwashing and isolation

  • Surveillance of intensive care unit infections, identification of new multidrug-resistant organisms, and appropriate use of antimicrobial therapy

  • Avoidance of unnecessary intubation and mechanical ventilation

  • Use of continuous positive airway pressure and BPAP, when possible

  • Use of correct pressure in endotracheal tube cuffs

  • Infection control techniques to prevent colonization of ventilator tubing circuits

  • Weaning patients off of ventilators in a timely fashion

  • Maintenance of adequate staffing levels in intensive care units

  • Maintenance of patients in a semi-upright position when intubated, especially when receiving enteral feeding

  • Routine prophylaxis with oral antibiotics (to decontaminate the digestive tract)

  • Use of prophylactic systemic antibiotics at the time of emergent intubation (being studied but not yet recommended)


All patients suspected of having ventilator-associated, hospital-acquired, or healthcare associated pneumonia should have an in-depth history and physical examination along with a chest x-ray [4]. Arterial oxygenation should be monitored to identify the need for supplemental oxygen. In addition, all patients with suspected ventilator-associated pneumonia should have blood cultures assessed. If the patient has a large or toxic appearing pleural effusion, diagnostic thoracentesis is indicated. Lower respiratory tract secretion (sputum) should be obtained prior to initiation of antibiotics and prior to changing antibiotics [4]. Sterile lower respiratory tract secretions in the absence of antibiotic therapy in the preceding 72 hours should be considered indicative of an absence of most bacterial pneumonia, but this does not rule out the possibility of Legionella or viral infection [4].


Guidelines for initial empiric therapy of hospital-acquired pneumonias state that patients without late onset (5 or fewer days) or any risk factors for multidrug-resistant pathogens should receive limited-spectrum antibiotic therapy, while patients with late-onset disease or risk factors for multidrug-resistant organisms should receive broad-spectrum antibiotic therapy [4]. Other guidelines for initial antibiotic therapy include [4]:

  • Choose specific agents based on local patterns of disease and resistance.

  • Treat patients with healthcare-associated pneumonia for potential multidrug-resistant infections.

  • Administer patients who have recently received a drug from another class of antibiotics.

  • Promptly administer initial antibiotic therapy.

  • Use antibiotics at optimal doses.

  • Consider aerosolized antibiotics in the treatment of ventilator-associated pneumonia with suspected multidrug-resistant, gram-negative infection.

  • Use combination therapy in patients with likely multidrug-resistant infection. Patients receiving combination therapy that includes an aminoglycoside can discontinue the aminoglycoside after 5 to 7 days.

  • Use monotherapy in patients with hospital-associated or ventilator-associated pneumonia who do not have infection caused by multidrug-resistant bacteria.

While the American Thoracic Society guidelines should be heavily weighted when making treatment decisions, these guidelines do not replace clinical judgment [4]. How to judge clinical response, when to broaden the therapy, and when to consider palliative care (especially in elderly dementia patients with aspiration pneumonia) are still clinical decisions, and no algorithm exists to come to the correct conclusions. These difficult decisions call for experienced, caring clinicians.


Multidrug-resistant pneumonia may develop in the community or healthcare settings, but it is most commonly a healthcare-associated, hospital-acquired, or ventilator-associated pneumonia [4]. According to the American Thoracic Society, possible pathogens in these patients include S. pneumoniae, H. influenzae, MRSA, P. aeruginosa, K. pneumoniae, Acinetobacter spp., and L. pneumophila [4]. A lower respiratory tract culture should be collected from all patients prior to the start of antibiotic therapy, but this should not delay the initiation of antibiotic therapy in critically ill patients [4]. Once data is available from lower respiratory tract cultures, therapy should be tailored (and unnecessary drugs eliminated) based on cultures and the patient's response to therapy. Early, appropriate, broad-spectrum antibiotic therapy at adequate dosage should be prescribed to optimize antimicrobial effect. If a patient has a history of recent antibiotic treatment, he or she should be started on therapy that includes antibiotics from a different class than that recently received. When treating vancomycin-sensitive multidrug-resistant organisms, linezolid is an alternative to vancomycin, and preliminary data suggest it may be clinically superior for ventilator-associated pneumonia due to MRSA [4]. Shorter therapy (7 to 8 days) should be considered for patients with uncomplicated hospital-acquired, ventilator-associated, or healthcare-associated pneumonia who have been placed on appropriate initial therapy and have had a good clinical response, as long as no evidence of infection with nonfermenting, gram-negative bacilli exists [4].

Aerosolized antibiotic therapy may be of value with patients diagnosed with ventilator-associated pneumonia due to carbapenem-resistant Acinetobacter bacteria [4]. When treating multidrug-resistant pneumonia due to P. aeruginosa, consideration should be given to short-term (5-day) treatment with an aminoglycoside in combination with a beta-lactam [4]. The four principles that underlie the management of hospital-acquired, ventilator-associated, or healthcare-associated pneumonia are [4]:

  • Avoid untreated or inadequately treated pneumonia, because the failure to initiate prompt, appropriate, and adequate therapy has been a consistent factor associated with increased mortality.

  • Recognize the variability of bacteriology from one hospital to another, specific sites within the hospital, and from one time period to another, and use this information to alter the selection of an appropriate antibiotic treatment regimen for any specific clinical setting.

  • Avoid the overuse of antibiotics by focusing on accurate diagnosis, tailoring therapy to the results of lower respiratory tract cultures, and shortening duration of therapy to the minimal effective period.

  • Apply prevention strategies aimed at modifiable risk factors.

The American Thoracic Society classifies risk factors for the development of hospital-acquired, ventilator-associated, or healthcare-associated pneumonia as modifiable or nonmodifiable and as patient-related (e.g., sex, age, pre-existing disease) or treatment-related (e.g., intubation, enteral feeding). The modifiable risk factors are the most obvious targets for improvement [4].


Vancomycin and linezolid are the only antibiotics approved by the FDA for the treatment of MRSA pneumonia. Other medications are currently available in Europe (including teicoplanin and quinupristin/dalfopristin), but these agents are not yet approved for manufacture and sale in the United States [45]. Ceftaroline fosamil (CPT-F), an antibiotic approved in 2010 by the FDA for treatment of bacterial infections, has shown promise for treatment of MRSA pneumonia. Researchers found that patients treated with CPT-F had a lower mortality rate after 28 days than patients treated with vancomycin [60].


Vancomycin is a glycopeptide antibiotic that is unique in its slow action. Given orally, vancomycin is not absorbed systemically; rather, it is excreted as unchanged drug, primarily in the feces. As such, its oral use is generally limited to the treatment of Clostridium difficile intestinal infections [45]. If this agent is used in the treatment of pneumonia and other nongastrointestinal infections, it is administered intravenously. However, vancomycin is actually less effective than beta-lactams in the treatment of MRSA infections [47]. It penetrates poorly into lung tissue, and despite in vitro tests showing susceptibility, poor penetration can lead to clinical failure. Vancomycin resistance was first documented in 1988, but complete resistance is still a fairly rare occurrence; intermediate resistance is now becoming an issue. Intermediate resistance is defined as a decreased area of inhibition (on an in vitro growth plate) at a given minimum inhibitory concentration (MIC). The MIC of a particular organism is defined as the lowest concentration of a particular drug that inhibits all visible growth of an organism (on an in vitro growth plate) under standard conditions. Therefore, an organism is resistant if its area of growth is large and its MIC is also high. An organism has intermediate resistance if there is excess growth, but not rising to the level of resistance, at a certain MIC. Furthermore, as currently defined, intermediate or "low-level" resistance is always an acquired characteristic, as the original organism must be susceptible to the antibiotic in question. Bacteria that are not naturally sensitive to an organism are simply defined as "resistant" to the antibiotic [48].

While vancomycin resistance is uncommon, an increase in MICs has been noted, which has been associated with increased mortality and treatment failure [47]. Vancomycin is also associated with side effects, notably nephrotoxicity and ototoxicity. The ideal dosing regimen of vancomycin maximizes the amount of drug received, but this may lead to an increase in side effects.

When prescribing vancomycin, the initial dosage is determined based on body weight, while the dosing interval is based on estimated creatinine clearance. The recommended dosage for MRSA pneumonia is 45–60 mg/kg daily to a maximum of 2 grams [45]. Doses of 1000 mg or less may be given over one hour, while doses of 1250 or greater may be given over 90 minutes.

Creatinine clearance (CrCl) can be estimated using the following formula [45,61]:

(140 – age) x ideal body weight (kg) divided by (72 x serum creatinine) = CrCl mL/min

To apply this calculation to women, the final number should be multiplied by 0.85. The calculation may then be used to determine dosing frequency (Table 4).


CrCl (mL/min)Dosing frequency
>80Every 12 hours
40–79Every 24 hours
25–39Every 48 hours
<25 or on hemodialysisGive an initial loading dose of 15–20 mg/kg, follow up dosing at 12–15 mg/kg when trough is <15 mcg/mL
Peritoneal dialysisConsult nephrologist due to variability

Most clinical guidelines call for monitoring drug levels only when treatment is expected to last longer than 4 days, the patient is receiving other nephrotoxic drugs, the patient is morbidly obese (i.e., weight considerably greater than 100 kg), or the patient has a severe, life-threatening infection; however, this may include many pneumonia patients [45]. Guidelines call for adjusting dosing of vancomycin based on trough levels obtained after the third dose and just prior to the fourth dose. Acceptable levels are considered to be between 15 and 20 mcg/mL, but research is ongoing as to optimal dosing [45]. Trough levels are considered important because low trough levels can lead to bacterial growth and are thought to lead to increased clinical failure and mortality [61].

When prescribing vancomycin, clinicians should be aware of potential adverse effects, including hypotension, flushing, and an erythematous rash referred to as "red man syndrome" (also "red neck syndrome"). Red man syndrome is one of two possible histamine-mediated hypersensitivity reactions, the other being anaphylaxis [62]. The incidence of red man syndrome ranges from 3.7% to 47%. Studies suggest that the incidence is higher in patients younger than 40 years of age and highest in children [62]. Some evidence suggests that the highest rates of red man syndrome occur in healthy individuals with no active infection [62]. It is hypothesized that the presence of infection causes a rise in histamine levels prior to the administration of vancomycin, which then down regulates the histamine response [62]. Red man syndrome is a rate-dependent infusion reaction (not a true allergic reaction) that is not thought to involve drug-specific antibodies. The syndrome occurs primarily with parenteral and first administration of vancomycin. Its occurrence following oral administration occurs primarily in patients with impaired renal function or other abnormalities [63]. Red man syndrome has been variously attributed to overly rapid infusion rate, impurities in the solution, and concomitant use of other antibiotics (e.g., ciprofloxacin, rifampin) or other medications (e.g., opioid analgesics, contrast dye) that may potentiate histamine release. Even after improvement in the purity of vancomycin, however, reports of the syndrome persist [64].

Red man syndrome generally consists of pruritus and an erythematous rash, with usual distribution on the face, neck, and upper torso [62,63]. Patients may develop dizziness, headache, and agitation as well as burning and itching. Signs and symptoms can develop as rapidly as 4 minutes after initiation of the infusion or as late as 7 days after initiation of therapy. Some reports have linked infusion times less than 1 hour with an increased incidence of red man syndrome [62].

Treatment of red man syndrome consists of discontinuation of the vancomycin infusion and administration of antihistamines [62]. Some clinicians advocate for regimens designed to decrease the incidence of red man syndrome; this includes administration of diphenhydramine 50 mg IV [62]. Other approaches add the H2 receptor antagonist cimetidine along with either diphenhydramine or hydroxyzine. If the rash and itching dissipate after treatment with diphenhydramine, the clinician can elect to restart the vancomycin infusion at a slower rate with close observation of the patient. This should only be done in a hospital setting where access to emergency care is immediately available.

As the diagnosis of red man syndrome can possibly cause the patient to be labeled "vancomycin allergic," it is paramount for the clinician to document any erythema that is present prior to infusion. This is especially true when cellulitis is present, as the patient may have a red, itchy rash at baseline.


Linezolid is a synthetic oxazolidinone that prevents binding of ribosomal subunits, thereby inhibiting protein synthesis. Compared to glycopeptides, linezolid achieves higher lung epithelial lining fluid concentrations. It has been hypothesized that linezolid may be clinically superior to vancomycin in the treatment of healthcare-associated pneumonia. However, a 2010 meta-analysis showed that linezolid was not clinically superior to either vancomycin or teicoplanin in the treatment of nosocomial pneumonia, and the lack of superiority was not influenced by the choice of glycopeptide drug [65].


Despite advances in treatment, pneumonia remains the leading cause of death in children younger than 5 years of age [66]. CAP is responsible for an estimated 20% of all deaths worldwide in this age group, with an especially heavy toll in developing countries, where 95% of all pediatric pneumonia deaths occur [13,67]. North America and Europe have an annual incidence of 40 cases per 1,000, highlighting the severity of pediatric pneumonia worldwide [68].


The WHO has defined pneumonia and its severity (and therefore subsequent treatment) according to clinical signs [69]. These guidelines are generally used in defining pediatric pneumonia, particularly in developing countries, and were revised in 2014. The revised WHO classification categories for pediatric pneumonia (children 2 to 59 months of age) are [67]:

  • No pneumonia: Cough and cold

  • Pneumonia: Fever and tachypnea and/or chest retraction

    • Children younger than 2 months: ≥60 breaths/min

    • Children 2 to 11 months: ≥50 breaths/min

    • Children 12 to 59 months: ≥40 breaths/min

  • Severe pneumonia or very severe disease: General danger signs (i.e., unable to drink, persistent vomiting, convulsions, lethargic or unconscious, stridor in calm child, severe malnutrition)

In developed countries, x-ray abnormalities are also used to determine a diagnosis and stage of disease.

Despite widespread acknowledgement of the problem of pediatric pneumonia, few epidemiologic studies are available to truly quantify the scope of the problem. Studies from the 1970s and 1980s show an incidence of 35 to 40 children younger than 5 years of age per 1000 population [70]. The number gradually decreases as children age, to 20 in 1000 for children 5 to 10 years of age and 10 in 1000 for children older than 10 years of age. Approximately 1% to 4% of all children are treated annually for CAP, and 0.1% to 2% of children are hospitalized annually for CAP [70].

Interestingly, the incidence of pediatric ambulatory CAP visits did not change significantly between 1994 and 2007, despite the introduction of heptavalent pneumococcal conjugate vaccine in 2000 [71]. There was, however, a decrease in the incidence of hospitalization for pediatric CAP over that same period. This may be due in part to lack of criteria for diagnosis of pneumonia in non-hospitalized pediatric patients [71].


The etiology of pediatric pneumonia differs from that in adults, with a higher incidence of viral pneumonias. Etiology also differs depending on location and vaccination status in the surrounding population. A 2009 European study examining causative agents in nonhospitalized pediatric patients with radiographic evidence of pneumonia found bacterial infection in 53% of patients and viral pathogens in 67% of patients, with 33% of children in the study showing evidence of both [68]. S. pneumoniae was the most common bacterial pathogen (46%); M. pneumoniae and C. pneumoniae were also isolated. Common viral infections included influenza A or B, parainfluenza, rhinovirus, RSV and, human metapneumovirus [68]. Other studies have supported this finding, showing a high rate of viral etiology in pediatric pneumonia patients (most often RSV and rhinovirus) [70]. Studies of hospitalized patients continue to show pneumococcal etiology in pediatric pneumonia patients, with S. pneumoniae the predominant causative agent [68]. Mycoplasma spp. also accounts for up to 14% of pneumonia in hospitalized pediatric patients.


One of the most common reasons for pediatric emergency room visits is fever, and fever is present in 88% to 96% of identified pneumonia cases in developed countries [70]. However, children with fever and wheezing commonly have either upper respiratory disease or reactive airway disease. While physical exam and history is important, obtaining a chest x-ray is important in the differential diagnosis of children with fever and respiratory symptoms and remains the gold standard for diagnosis [70]. In a 2009 study of 99 children hospitalized with what was later determined to be pneumonia, the most common abnormal finding was "diminished" breath sounds; only 21% were described as having "normal" breath sounds [68]. Radiologic consolidation was present in 79% of patients, and correlation between diminished breath sounds and radiologic consolidation was 60.2% [68].

In the absence of chest x-ray (especially frequent in developing countries), the clinician should be aware of subtle signs and symptoms of pneumonia in the pediatric patient. Diminished breath sounds and fine end-inspiratory crackles may be signs of pneumonia. In one study, non-specific crackles were present in more than 90% of children with pneumococcal or mycoplasmal pneumonia [70]. Other studies have emphasized the role of non-specific signs and symptoms, such as vomiting and abdominal pain, in making diagnoses in pediatric patients [70]. Newborns with pneumonia commonly present with poor feeding and irritability as well as tachypnea, retractions, grunting, and hypoxemia; cough is rare [64].


While the treatment of healthcare-associated pneumonia is similar regardless of age group, specific guidelines have been established for the treatment of CAP in pediatric patients. As discussed, the most frequent cause of pediatric CAP is S. pneumoniae. Prescribing patterns are not as standardized as in adult pneumonia, and despite lack of evidence of superiority to penicillin, macrolides were the most frequently prescribed antibiotic for pediatric CAP in 2007 (34% of patients) [71]. The second most frequent were cephalosporins (22%), and penicillins were third most frequently prescribed (14%). Cephalosporin use increased significantly between 2000 and 2007.

The 2014 WHO guidelines call for patients 2 months to 5 years of age with severe CAP to be hospitalized and treated with parenteral antibiotics and supportive therapy [67]. In 2011, the Pediatric Infectious Diseases Society and the IDSA established clinical guidelines for the management of CAP in otherwise healthy infants and children older than 3 months of age [66]. These guidelines recommend that the presence of any of the following in a child with pneumonia necessitates hospitalization [66]:

  • Moderate-to-severe CAP, as defined by several features, including respiratory distress and hypoxia

  • Age younger than 3 to 6 months with suspected bacterial CAP

  • CAP suspected or documented to be caused by a pathogen with increased virulence (e.g., CA-MRSA)

  • Concern regarding observation or compliance with prescribed treatment protocols

Because most cases of pneumonia in young children are the result of viral rather than bacterial infection, empiric antimicrobial therapy should not be initiated in these patients. However, for pediatric patients with suspected mild-to-moderate bacterial pneumonia, amoxicillin is considered the first-line therapy [66,67]. Amoxicillin provides coverage of several pathogens, including S. pneumoniae, the most common invasive bacterial pathogen [66]. During influenza season, pediatric patients with moderate-to-severe CAP consistent with influenza infection should be started on antiviral medication as soon as possible. Finally, for patients with documented atypical pneumonia syndrome, a macrolide antibiotic (azithromycin) is the first choice [66]. Treatment should continue for 10 days, although certain pathogens, such as CA-MRSA, require longer courses of treatment.


As discussed, P. jiroveci pneumonia is a fungal infection of the lungs. This organism is common in the environment and does not typically cause disease in immunocompetent patients; however, among patients with compromised immune systems, P. jiroveci pneumonia can be devastating. This includes the elderly, severely malnourished children, extremely premature infants, patients taking chemotherapy, patients on long-term corticosteroid therapy, solid organ or bone marrow transplantation recipients, and particularly individuals with HIV infection [22]. For persons with HIV, P. jiroveci pneumonia is the most common opportunistic infection and a signal that the patient has progressed to AIDS.

Pneumocystis is commonly found in the lungs of healthy individuals, and more than 75% of all children are seropositive by 4 years of age, although clinical disease is rare [72]. Clinical cases of P. jiroveci pneumonia have been described on all continents, except Antarctica.


P. jiroveci infection causes fever, dry cough, weight loss, and shortness of breath. There is a lack of sputum production present in many other pneumonias due to the high viscosity of the sputum.

Chest x-ray in patients with P. jiroveci infection reveals widespread pulmonary infiltrates. Blood gas analysis reveals low arterial oxygenation. Confirmation is made by sputum culture, if sputum can be obtained.


The first-line treatment of P. jiroveci pneumonia is TMP-SMX, with dosing of 5 mg/kg of TMP and 25 mg/kg of SMX every 6 to 8 hours, either orally or IV [45,73]. Alternative regimens include TMP 5 mg/kg every 6 to 8 hours plus dapsone 100 mg daily, atovaquone 750 mg twice daily, or trimetrexate 45 mg/m2 daily IV plus leucovorin 20 mg/kg every 6 hours orally or IV [6,45].

Patient education should concentrate on the need for strict adherence to the chosen prophylaxis regimen, as well as adherence to all medications. Further patient education should help the patient identify the early signs and symptoms of infection.

Prevention of P. jiroveci is primarily accomplished by identifying high-risk patients and placing them on standard prophylaxis regimens. The approved preventative regimen is TMP-SMX, either one double-strength or single-strength tablet daily [45,73]. Alternative regimens are oral dapsone 50 mg twice daily or 100 mg daily, dapsone 50 mg per day plus pyrimethamine (50 mg) and leucovorin (25 mg) weekly. Leucovorin prevents bone marrow toxicity from pyrimethamine. Finally, weekly dapsone (200 mg/week) plus pyrimethamine (75 mg) and leucovorin (25 mg) may be considered, particularly for patients with compliance issues who are on directly observed therapy. Pentamidine 300 mg monthly via an approved nebulizer system is also an alternative prophylaxis regimen [6].


Approximately 200 million cases of community-acquired viral pneumonia occur every year, with an equal number affecting children and adults (although mortality rates vary among these groups) [12]. Molecular diagnostics have increased general knowledge of the role of viruses in pneumonia, and up to 50% of all cases of CAP in adults are now believed to be viral in origin [12]. RSV is the most common cause of viral pneumonia in infants and children [74]. Other common causes include rhinovirus, human metapneumovirus, human bocavirus, and parainfluenza virus [12]. Although a rare cause of pneumonia in healthy young adults, viral pneumonia is a significant issue among elderly and immunocompromised patients [74]. In adults, the most common causative organisms are influenza types A and B, which account for more than 50% of all cases of CAP [74]. Other causative organisms include rhinovirus, CoV, influenza virus, RSV, adenovirus, and parainfluenza virus [12,75]. The development of vaccines against bacterial pneumonias has led to an increase in the role of viruses, especially in pediatric pneumonia cases. Pandemics of H1N1 influenza and SARS have emphasized the public health threat from viral outbreaks.


While the diagnosis of pneumonia remains based primarily on clinical features (i.e., cough, sputum, fever, and chest x-ray changes), the diagnosis of a viral etiology is made by detection of a virus or viral antigen in nasopharyngeal or sputum specimens [12]. Because this method takes a long time to complete, faster methods, such as viral-antigen detection, have been introduced [74]. Polymerase chain reaction (PCR) techniques have allowed laboratories to directly detect respiratory viruses. However, diagnosis can be complicated by chronic colonization, prolonged shedding, and difficulty in obtaining true lower respiratory tract samples [74]. These limitations can be overcome by the use of quantitative PCR, which shows the level of viral load and can help in differentiating active infection from contamination [74]. Diagnosis of community-acquired viral pneumonia is also complicated by the fact that the majority of research has been done on hospitalized patients.

Factors suggestive of a viral origin include patient age younger than 5 years of age, viral epidemic in the community, slow onset of disease, rhinitis, chest x-ray findings of bilateral interstitial infiltrates, fever less than 38.5°C, and slow or no response to antibiotics [12]. White blood cell count may be lower than that seen in bacterial pneumonia, generally staying below 10 x 109/Liter [12]. The American Thoracic Society emphasizes chest x-ray findings in the diagnosis of viral pneumonia, stating that interstitial infiltrates (as opposed to the classic lobar infiltrate) indicate a diagnosis of viral etiology. A study of comorbid conditions among a population of 4277 children with pneumonia in Finland found a high concurrence of other conditions in certain viral pneumonia syndromes [12,76]. Specifically, otitis media was found in 59% of children with RSV and in 77% if parainfluenza virus infections. Some co-infections were significantly associated with particular viruses, with laryngitis occurring almost exclusively with parainfluenza viral pneumonias and tonsillitis strongly correlated with pneumonia caused by adenovirus [76].

When obtaining a culture the clinician should generally order a nasopharyngeal swab, which has a higher sensitivity than throat swabs. Swabs should be taken at a depth of 2 to 3 cm. It is important to note that nasopharyngeal swabs are generally not sensitive for RSV.


Treatment methods for viral infection have increased since 1990, but options are still limited. Neuraminidase inhibitors, including oseltamivir, zanamivir, and peramivir, are the mainstay of treatment of most viral infections, particularly pneumonia caused by influenza [2,12,74]. However, viral resistance is a concern, and it is unclear when or if these agents should be used in cases of community-acquired viral pneumonia. In addition, the role of antibiotics in treating pneumonia of viral origin is undetermined [12]. All patients with viral pneumonia should receive supportive care with oxygen, rest, antipyretics, analgesics, nutrition, and close observation [74].

Prevention of viral pneumonia should focus on vaccination and awareness of outbreaks and guidelines regarding prophylaxis during outbreaks of exposed high-risk individuals. Adhering to good hand hygiene and cough cover practices can help decrease the spread of viral diseases.



Patient A, a man 58 years of age, presents to the walk-in clinic complaining of a 24-hour history of fever and chills, with an episode of rigors last night. He has previous history that is significant for COPD, diabetes, and a 2 pack per day smoking habit and a lifetime pack year history greater than 75 years. His medications include a combination steroid/long-acting beta agonist inhaler, tiotropium bromide and albuterol, as needed. He complains of increased dyspnea and has been using his inhaler almost constantly. He admits to a productive cough but is not sure if it is much different than his normal "smoker's cough," as he calls it. The office medical technologist obtains vital signs, and Patient A has a blood pressure of 168/92 mm Hg, a pulse of 128 beats per minute, a respiratory rate of 32 breaths per minute, and a pulse oximetry on room air of 87%. His temperature (taken with a forehead "tape" thermometer) is 97.5°F. The patient is placed on 4 liters O2 and given an albuterol solution via small volume nebulizer. His O2 saturation increases to 94%, his respiratory rate decreases to 24 breaths per minute, and his pulse decreased to 112 beats per minute.

Comments and rationale: At this point, the differential includes exacerbation of COPD, acute viral syndrome, viral pneumonia, and bacterial pneumonia. A few actions can help quickly limit the differential. The first is to determine if Patient A is sweaty. A very recent defervescence could cause a wide discrepancy between rectal and tympanic temperatures versus methods that measure skin temperature. The cooling effect of sweat will cause an underestimation of the patient's true body temperature. The patient's tympanic temperature would likely be more accurate in this situation.

Next, lung sounds should be assessed, with percussion and full examination for egophony and fremitus performed. The presence of abnormal sounds would alert the clinician to do a more thorough exam. Finally, if the clinician is convinced that the patient likely has CAP, the decision whether or not to hospitalize must be made.

A tympanic probe displays a temperature of 101.3°F. Auscultation of lung sounds reveals fremitus as well as expiratory wheezes and rhonchi. As Patient A is still mildly hypoxic (as well as tachypneic and tachycardic) and requiring supplemental oxygen, the decision is made to transport to the local hospital via emergency medical services. There, a chest x-ray reveals a right lower lobe infiltrate and a white blood cell count of 17,000/mm3. Sputum culture reveals S. pneumoniae. The patient is placed on moxifloxacin 400 mg daily for 7 days and is started on prednisone and albuterol via small-volume nebulizer. Patient A rapidly improves and is discharged 3 days later with instructions to finish his antibiotics and steroids and to follow-up with his primary care practitioner.

Comments and rationale: Patient A represents a typical case of CAP, with relatively common underlying risk factors (COPD, smoking, and diabetes). While his hospitalization was short due to rapid identification of his pneumonia, he now requires outpatient follow-up to avoid relapse and to decrease his risk for recurrence. Intensive treatment for smoking cessation is warranted, and he may need adjustment of his insulin regimen while on steroids. Another factor to consider is how long to follow his chest x-ray. Many clinicians advocate serial x-rays until the pneumonia is completely resolved, to eliminate the possibility of an underlying carcinoma causing a chronic infiltrate. As this patient is very high risk for lung cancer, this may be a reasonable strategy. A persistent infiltrate would require further work-up.


Patient B is a man, 82 years of age, living in a nursing home. He has COPD, a history of smoking, mild dementia, and hypertension. One morning, his caregivers note that he has a temperature of 101°F and is mildly obtunded and confused. His oxygen saturation as obtained by pulse oximetry is 88%. His primary care practitioner is called and an order is obtained to transfer him to an acute care facility. While in the emergency department, sputum for culture, sensitivity, and Gram stain is obtained. Lab work including a white blood cell count is sent, and a chest x-ray is obtained.

Comments and rationale: Healthcare-associated pneumonia can be caused by a wide variety of pathogens, including multidrug-resistant, aerobic, gram-negative bacteria such as P. aeruginosa, E. coli, K. pneumoniae, and Acinetobacter spp. Potential gram-positive causative organisms include S. aureus, and the potential for a methicillin-resistant strain is significant. While it should not delay care, all patients with suspected pneumonia should have a lower respiratory tract sample sent for culture and microscopic evaluation. Diagnostic testing is ordered both to determine if the patient's symptoms are the result of pneumonia and to determine the causative pathogen.

Patient B's chest x-ray reveals a new right lower lobe infiltrate, and his white blood cell count is 18,000/mm3. His temperature is 101°F, and he is noted to have purulent sputum. A diagnosis of healthcare-associated pneumonia is made, and the patient is started on moxifloxacin 400 mg per day. He is placed on supplemental oxygen via nasal cannula to maintain an oxygen saturation of 90% or greater.

Comments and rationale: The clinical diagnosis of pneumonia is generally defined as the presence of a new infiltrate on chest x-ray and at least two or three clinical symptoms (in Patient B's case, fever, leukocytosis, and purulent secretions). The selection of appropriate initial antibiotic therapy is key in reducing morbidity and mortality.

The patient's fever increases to 102°F, and he now requires 40% ventilation mask to maintain adequate oxygenation. He is moved to the ICU, and the hospital laboratory reports initial findings on the patient's sputum culture. The sputum is found to contain a predominant strain of gram-positive organism. Due to the patient's failure to improve on a quinolone and the presence of gram-positive bacteria, the decision is made to change the patient's antibiotic regimen to a broad-spectrum regimen designed to cover multidrug-resistant organisms. Patient B is placed on vancomycin 1 gram IV every 12 hours, with orders to check a trough level one hour after the third dose. He is also placed on piperacillin and tazobactam and intravenous levofloxacin, in accordance with the American Thoracic Society's guidelines for the treatment of patients with healthcare-associated pneumonia with risk factors for multidrug-resistant pathogens [4].

Comments and rationale: Only vancomycin and linezolid are currently approved for use in the United States to treat MRSA pneumonia. Although TMP-SMX often has significant activity against MRSA, its use should be limited to mild disease, such as urinary tract infection not causing sepsis. As the causative agent is rarely identified prior to initial antibiotic dosing, the type of pneumonia and the patient's known risk factors are used to guide antibiotic selection.

In this case, the patient is failing to improve, and the Gram stain is able to provide guidance regarding tailoring the individual antibiotic regimen. After the patient has been identified as having healthcare-associated pneumonia, likely due to a drug-resistant organism, the decision must be made whether and how to use broad-spectrum antibiotics. Although all clinicians should strive to avoid inappropriate initial selection when ordering antibiotic therapy, this case presents the dilemma faced in treating a patient whose only known initial risk factor was residing in a nursing home. The American Thoracic Society guidelines state that initial empiric antibiotic therapy for these patients can be ceftriaxone or a respiratory quinolone, or ampicillin/sulbactam or ertapenem. The patient was initially treated with a respiratory quinolone, and therefore, his initial treatment was appropriate. However, after information was obtained that the causative organism was likely a gram-positive organism and the patient was noted to be deteriorating, his antibiotic regimen was broadened to include protection against multidrug-resistant organisms, especially MRSA. Length of therapy can vary depending on the rate of improvement, but generally the patient should be on the appropriate antibiotic for 7 days.

Patient B gradually improves, and after 72 hours, the cultures are found to be positive for MRSA. His antibiotic regimen is tailored to these findings, and he is placed solely on IV vancomycin.


Patient C is a community-dwelling woman, 58 years of age, with a history of asthma and diabetes. She presents to an urgent care facility with a 48-hour history of cough, fever, and wheezing. On exam, her vital signs are: blood pressure 154/78 mm Hg; pulse 94 beats per minute; respirations 24 breaths per minute; and temperature 99.4°F. Her oxygen saturation is 93% on room air. Her usual medications are fluticasone/salmeterol, metformin, lisinopril, and albuterol (as needed). A chest x-ray reveals a small infiltrate in the right lower lobe, and a diagnosis of CAP is made. Patient C is given a prescription for levofloxacin 500 mg twice daily, prednisone 40 mg with a tapering schedule calling for a decrease in dosage by 5 mg every other day, and instructions to take acetaminophen for fever and guaifenesin for cough. She is instructed to follow up with her primary care clinician in 24 to 48 hours and to seek immediate emergency treatment for worsening of symptoms.

Comments and rationale: Given this patient's comorbidities, an initial choice of a respiratory fluoroquinolone is a good one. The patient has several pre-existing conditions that could complicate her care, and antibiotic failure would leave her susceptible for a poor clinical outcome. It is unclear if the clinician checked the patient's renal status via a blood test for BUN and serum creatinine. Levofloxacin is excreted via the kidney, and diabetic patients like Patient C are at increased risk for developing chronic kidney disease, which could lead to acute renal failure in the presence of dehydration. Further complicating Patient C's care is the fact that steroid therapy often results in worsening glycemic control, which can lead to polyuria and further exacerbate dehydration.

Patient C continues to have wheezing despite the use of her albuterol inhaler. Her condition worsens until she contacts emergency medical services and is transported via ambulance to a local hospital. Her vital signs in the emergency department are: blood pressure 104/53 mm Hg; pulse 115 beats per minute; respirations 28 breaths per minute; temperature 99.3°F; and oxygen saturation 89%. Auscultation of her lungs reveals inspiratory and expiratory wheezing with diminished air flow as well as decreased breath sounds at the right base. Patient C is placed on supplemental oxygen and given hydrocortisone sodium succinate 150 mg IV. Laboratory studies are sent and reveal an arterial blood gas of pH 7.41, arterial carbon dioxide tension of 45 mm Hg, and pulmonary arterial oxygen tension of 55 mm Hg. Her serum glucose is 235 mg/dL, BUN 53 mg/dL, and serum creatinine of 2.8 mg/dL. She is placed on IV fluid of D5 ½ at 150 mL per hour. The patient's lisinopril and metformin are placed on hold, and an insulin sliding scale is ordered. A chest x-ray again reveals a right lower lobe infiltrate. She is continued on oral levofloxacin, but the dose is decreased based on her renal function, and sputum for Gram stain as well as culture and sensitivity is sent. Patient C also has blood cultures drawn. She is admitted with diagnosis of CAP, exacerbation of asthma, diabetes, dehydration, and mild acute renal failure. She is placed on albuterol nebulizer treatments every 4 hours or more often as needed, and she is given heparin 5000 units subcutaneously for deep vein thrombosis prophylaxis.

Comments and rationale: Patient C represents a case in which the initial antibiotic therapy was correct, but the patient's pre-existing conditions and severity of illness made continued outpatient therapy unwise. Physician consultation is always recommended for patients with oxygen saturations of less than 90% on room air, rigors, changes in mental status, abnormal vital signs, or comorbid disease (e.g., diabetes, HIV, cancer, or COPD).


Pneumonia can range from a simple, non-life-threatening infection to a complex case of multidrug-resistant, healthcare-associated pneumonia. Pneumonia remains a leading cause of worldwide morbidity and mortality, and successful treatment requires clinicians to have knowledge of both current guidelines and local patterns of resistance and epidemiology. Emerging threats in the form of developing resistances, new pathogens, and an aging patient population are causing many researchers and clinicians to consider the possibility of pneumonia again becoming a major public health issue in the United States. Primary care clinicians are on the front line of disease prevention and, through widespread use of vaccines and judicious use of available antibiotics, can help win the war against this ancient disease.


Alliance for the Prudent Use of Antibiotics
American Lung Association
American Society for Microbiology
American Thoracic Society
Centers for Disease Control and Prevention
Infectious Diseases Society of America
U.S. Food and Drug Administration Center for Drug Evaluation and Research
World Health Organization

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Evidence-Based Practice Recommendations Citations

1. Kirsch J, Mohammed TH, Kanne JP, et al. ACR Appropriateness Criteria: Acute Respiratory Illness in Immunocompetent Patients. Reston, VA: American College of Radiology; 2013. Summary retrieved from National Guideline Clearinghouse at http://www.guideline.gov/content.aspx?id=47676. Last accessed May 22, 2015.

2. Centers for Disease Control and Prevention, Advisory Committee on Immunization Practices. Updated recommendations for prevention of invasive pneumococcal disease among adults using the 23-valent pneumococcal polysaccharide vaccine (PPSV23). MMWR. 2010;59(34):1102-1106. Summary retrieved from National Guideline Clearinghouse at http://www.guideline.gov/content.aspx?id=24164. Last accessed May 22, 2015.

3. Institute for Clinical Systems Improvement. Prevention of Ventilator-Associated Pneumonia. Bloomington, MN: Institute for Clinical Systems Improvement; 2011. Summary retrieved from National Guideline Clearinghouse at http://www.guideline.gov/content.aspx?id=36063. Last accessed May 22, 2015.

4. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the Infectious Diseases Society of America for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis. 2011;52:1-38. Summary retrieved from National Guideline Clearinghouse at http://www.guideline.gov/content.aspx?id=25412. Last accessed May 22, 2015.

5. Bradley JS, Byington CL, Shah SS, et al. The management of community-acquired pneumonia in infants and children older than 3 months of age: clinical practice guidelines by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America. Clin Infect Dis. 2011;53(7):e25-e76. Summary retrieved from National Guideline Clearinghouse at http://www.guideline.gov/content.aspx?id=34433. Last accessed May 22, 2015.

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