case presentation on pneumonia

• Search Menu
• Advance articles
• Editor's Choice
• Supplement Archive
• Cover Archive
• IDSA Guidelines
• IDSA Journals
• The Journal of Infectious Diseases
• Open Forum Infectious Diseases
• Photo Quizzes
• State-of-the-Art Reviews
• Voices of ID
• Author Guidelines
• Open Access
• Why Publish
• Advertising and Corporate Services
• Advertising
• Journals Career Network
• Reprints and ePrints
• Sponsored Supplements
• Branded Books
• About Clinical Infectious Diseases
• About the Infectious Diseases Society of America
• About the HIV Medicine Association
• IDSA COI Policy
• Editorial Board
• Self-Archiving Policy
• For Reviewers
• For Press Offices
• Journals on Oxford Academic
• Books on Oxford Academic

Article Contents

Case presentation, acknowledgments.

• < Previous

Scenario 1: A Patient with Mild Community-Acquired Pneumonia—Introduction to Clinical Trial Design Issues

• Article contents
• Figures & tables
• Supplementary Data

David N. Gilbert, Scenario 1: A Patient with Mild Community-Acquired Pneumonia—Introduction to Clinical Trial Design Issues, Clinical Infectious Diseases , Volume 47, Issue Supplement_3, December 2008, Pages S121–S122, https://doi.org/10.1086/591391

• Permissions Icon Permissions

A prototypical patient is presented to introduce important design issues for clinical trials of antibacterials in the treatment of community-acquired pneumonia.

Of the 4 million or more patients in the United States treated annually for community-acquired pneumonia (CAP), ∼80% are cared for on an outpatient basis [ 1 , 2 ]. Admittedly, the patient population is heterogeneous. However, 2 subgroups constitute a significant percentage of the total.

The first subgroup consists of young, otherwise-healthy individuals who are nonsmokers aged <40 years. “Atypical” pathogens, such as Mycoplasma pneumoniae or Chlamydia pneumoniae , are identified frequently as the etiologic organism. Streptococcus pneumoniae may be the etiologic organism, especially during or after viral tracheobronchitis.

In contrast, individuals in the second group are older. Often, they have used tobacco products for years and meet clinical criteria for chronic bronchitis and/or emphysema.

To focus on clinical trial design issues pertinent to the population of patients with mild pneumonia, a typical clinical-trial candidate patient is described below.

Present illness. A 35-year-old male resident of Boston, Massachusetts, presents with fever and cough. He was well until 3 days earlier, when he suffered the onset of nasal stuffiness, mild sore throat, and a cough productive of small amounts of clear sputum. Today, he decided to seek physician assistance because of an increase in temperature to 38.3°C and spasms of coughing that produce purulent secretions. On one occasion, he noted a few flecks of bright-red blood in his sputum.

Other pertinent history. It is March. He lives in a home in the city with his wife and 3 children, aged 7, 9, and 11 years. The children are fully immunized. The 11-year-old child is recovering from a “nagging” cough that has persisted for 10–14 days.

The family has a pet parakeet who is 5 years old and appears to be well. The patient has not traveled outside the city in the past year. He is an office manager.

The patient smokes 1 pack/day and has done so since the age of 15 years. Several times a month, especially during the winter, on arising from sleep, he produces ∼1 tablespoon of purulent sputum.

Medical history. The patient has no history of familial illness, hospitalizations, or trauma. There are no drug allergies or intolerance. The only medication he takes is acetaminophen occasionally, for headaches. He drinks beer or wine in moderation.

Physical examination. His body temperature is 38.9°C (100°F), his pulse is 110 beats/min and regular, and his respiratory rate is 18 breaths/min. His oxygen saturation is 93% while breathing room air. There is mild erythema of the mucosa of the nose and posterior oropharynx. Inspiratory “rales” are heard at the right lung base.

Laboratory and radiographic findings. His hemoglobin level is 12.5 g/dL, with a hematocrit of 36%. His WBC count is 13,500 cells/µL, with 82% polymorphonuclear cells, 11% band forms, and 7% lymphocytes. His platelet count is 180,000 cells/µL. The results of a multichemistry screen are unremarkable.

Chest radiography documents bilateral lower lobe infiltrates that are more pronounced on the right side. There are no pleural effusions.

Management questions. A validated prediction rule forecasts that this patient's risk of death from his CAP is <1% [ 3 ]. Therefore, he is a candidate for outpatient therapy.

What is the likely microbiological diagnosis? On the basis of the cough of 2 weeks' duration in the patient's 11-year-old child, the pneumonia could be due to M. pneumoniae or another atypical pathogen. However, this illness could represent pneumococcal pneumonia superimposed on a viral upper respiratory tract infection.

Clinical trial design questions. These are the hard questions and illustrate some of the many reasons for this workshop: Is the patient of sufficient reliability to participate in an outpatient clinical trial of antibacterials for mild CAP? Is it ethical or, from a practical standpoint, feasible to conduct a placebo-controlled trial? If an active comparator drug is used, how does one generate a valid and defensible margin of noninferiority?

What are valid, reproducible, and quantifiable clinical end points (outcomes)?

It would help greatly if the etiology of the pneumonia could be determined for the majority of the enrolled patients. What are the current diagnostic tools that can be applied and thereby “enrich” the patient population?

Multiple precautions are necessary to avoid bias in the interpretation of the results of clinical trials. For example, what are acceptable methods in the “blinding” of treatment arms?

How can investigators reliably and with reasonable sensitivity detect adverse drug effects?

The articles that follow address these questions and more. Participants in this workshop uniformly agreed that the interaction of US Food and Drug Administration regulations, industry sponsors, and Infectious Diseases Society of America academics represents an opportunity to modernize future clinical trials for CAP.

Supplement sponsorship. This article was published as part of a supplement entitled “Workshop on Issues in the Design and Conduct of Clinical Trials of Antibacterial Drugs for the Treatment of Community-Acquired Pneumonia,” sponsored by the US Food and Drug Administration and the Infectious Diseases Society of America.

Potential conflicts of interest. D.N.G. serves on the speakers' bureau of Abbott Laboratories, Bayer, GlaxoSmithKline, Lilly, Merck, Pfizer, Roche, Schering-Plough, and Wyeth; and has received consulting fees from Advanced Life Sciences and Pacific Beach Bioscience.

Google Scholar

• community acquired pneumonia
• anti-bacterial agents

Email alerts

More on this topic, related articles in pubmed, citing articles via, looking for your next opportunity.

• Recommend to your Library

Affiliations

• Online ISSN 1537-6591
• Print ISSN 1058-4838
• Copyright © 2024 Infectious Diseases Society of America
• About Oxford Academic
• Publish journals with us
• University press partners
• What we publish
• New features  
• Open access
• Institutional account management
• Rights and permissions
• Get help with access
• Accessibility
• Media enquiries
• Oxford University Press
• Oxford Languages
• University of Oxford

Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide

• Copyright © 2024 Oxford University Press
• Cookie settings
• Cookie policy
• Privacy policy
• Legal notice

This Feature Is Available To Subscribers Only

Sign In or Create an Account

This PDF is available to Subscribers Only

For full access to this pdf, sign in to an existing account, or purchase an annual subscription.

Learn how UpToDate can help you.

Select the option that best describes you

• Medical Professional
• Resident, Fellow, or Student
• Hospital or Institution
• Group Practice
• Patient or Caregiver
• Find in topic

CALCULATORS

Related pathways, related topics.

Contributor Disclosures

Please read the Disclaimer at the end of this page.

INTRODUCTION  —  Community-acquired pneumonia (CAP) is a leading cause of morbidity and mortality worldwide. The clinical presentation of CAP varies, ranging from mild pneumonia characterized by fever and productive cough to severe pneumonia characterized by respiratory distress and sepsis. Because of the wide spectrum of associated clinical features, CAP is a part of the differential diagnosis of nearly all respiratory illnesses.

This topic provides a broad overview of the epidemiology, microbiology, pathogenesis, clinical features, diagnosis, and management of CAP in immunocompetent adults. Detailed discussions of each of these issues are presented separately; links to these discussions are provided within the text below.

DEFINITIONS  —  Pneumonia is frequently categorized based on site of acquisition ( table 1 ).

● Community-acquired pneumonia (CAP) refers to an acute infection of the pulmonary parenchyma acquired outside of the hospital.

● Nosocomial pneumonia refers to an acute infection of the pulmonary parenchyma acquired in hospital settings and encompasses both hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP).

• HAP refers to pneumonia acquired ≥48 hours after hospital admission.

• VAP refers to pneumonia acquired ≥48 hours after endotracheal intubation.

Health care-associated pneumonia (HCAP; no longer used) referred to pneumonia acquired in health care facilities (eg, nursing homes, hemodialysis centers) or after recent hospitalization. The term HCAP was used to identify patients at risk for infection with multidrug-resistant pathogens. However, this categorization may have been overly sensitive, leading to increased, inappropriately broad antibiotic use and was thus retired. In general, patients previously classified as having HCAP should be treated similarly to those with CAP. (See "Epidemiology, pathogenesis, microbiology, and diagnosis of hospital-acquired and ventilator-associated pneumonia in adults" .)

EPIDEMIOLOGY

Incidence  —  CAP is one of the most common and morbid conditions encountered in clinical practice [ 1-3 ]. In the United States, CAP accounts for over 4.5 million outpatient and emergency room visits annually, corresponding to approximately 0.4 percent of all encounters [ 4 ]. CAP is the second most common cause of hospitalization and the most common infectious cause of death [ 5,6 ]. Approximately 650 adults are hospitalized with CAP every year per 100,000 population in the United States, corresponding to 1.5 million unique CAP hospitalizations each year [ 7 ]. Nearly 9 percent of patients hospitalized with CAP will be rehospitalized due to a new episode of CAP during the same year.

Risk factors

● Older age – The risk of CAP rises with age [ 7,8 ]. The annual incidence of hospitalization for CAP among adults ≥65 years old is approximately 2000 per 100,000 in the United States [ 7,9 ]. This figure is approximately three times higher than the general population and indicates that 2 percent of the older adult population will be hospitalized for CAP annually ( figure 1 ).

● Chronic comorbidities – The comorbidity that places patients at highest risk for CAP hospitalization is chronic obstructive pulmonary disease (COPD), with an annual incidence of 5832 per 100,000 in the United States [ 7 ]. Other comorbidities associated with an increased incidence of CAP include other forms of chronic lung disease (eg, bronchiectasis, asthma), chronic heart disease (particularly congestive heart failure), stroke, diabetes mellitus, malnutrition, and immunocompromising conditions ( figure 2 ) [ 7,10,11 ].

● Viral respiratory tract infection – Viral respiratory tract infections can lead to primary viral pneumonias and also predispose to secondary bacterial pneumonia. This is most pronounced for influenza virus infection. (See "Seasonal influenza in adults: Clinical manifestations and diagnosis", section on 'Pneumonia' .)

● Impaired airway protection – Conditions that increase risk of macroaspiration of stomach contents and/or microaspiration of upper airway secretions predispose to CAP, such as alteration in consciousness (eg, due to stroke, seizure, anesthesia, drug or alcohol use) or dysphagia due to esophageal lesions or dysmotility.

● Smoking and alcohol overuse – Smoking, alcohol overuse (eg, >80 g/day), and opioid use are key modifiable behavioral risk factors for CAP [ 7,10,12,13 ].

● Other lifestyle factors – Other factors that have been associated with an increased risk of CAP include crowded living conditions (eg, prisons, homeless shelters), residence in low-income settings, and exposure to environmental toxins (eg, solvents, paints, or gasoline) [ 7,10,11,14 ].

Combinations of risk factors, such as smoking, COPD, and congestive heart failure, are additive in terms of risk [ 15 ]. These risk factors and other predisposing conditions for the development of CAP are discussed separately. (See "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults", section on 'Predisposing host conditions' .)

MICROBIOLOGY

Common causes  —  Streptococcus pneumoniae (pneumococcus) and respiratory viruses are the most frequently detected pathogens in patients with CAP [ 8,16 ]. However, in a large proportion of cases (up to 62 percent in some studies performed in hospital settings), no pathogen is detected despite extensive microbiologic evaluation [ 8,17,18 ].

The most commonly identified causes of CAP can be grouped into three categories:

● Typical bacteria

• S. pneumoniae (most common bacterial cause)

• Haemophilus influenzae

• Moraxella catarrhalis

• Staphylococcus aureus

• Group A streptococci

• Aerobic gram-negative bacteria (eg, Enterobacteriaceae such as Klebsiella spp or Escherichia coli )

• Microaerophilic bacteria and anaerobes (associated with aspiration)

● Atypical bacteria ("atypical" refers to the intrinsic resistance of these organisms to beta-lactams and their inability to be visualized on Gram stain or cultured using traditional techniques)

• Legionella spp

• Mycoplasma pneumoniae

• Chlamydia pneumoniae

• Chlamydia psittaci

• Coxiella burnetii

● Respiratory viruses

• Influenza A and B viruses

• Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)

• Other coronaviruses (eg, CoV-229E, CoV-NL63, CoV-OC43, CoV-HKU1)

• Rhinoviruses

• Parainfluenza viruses

• Adenoviruses

• Respiratory syncytial virus

• Human metapneumovirus

• Human bocaviruses

The relative prevalence of these pathogens varies with geography, pneumococcal vaccination rates, host risk factors (eg, smoking), season, and pneumonia severity ( table 2 ).

Certain epidemiologic exposures also raise the likelihood of infection with a particular pathogen ( table 3 ). As examples, exposure to contaminated water is a risk factor for Legionella infection, exposure to birds raises the possibility of C. psittaci infection, travel or residence in the southwestern United States should raise suspicion for coccidioidomycosis, and poor dental hygiene may predispose patients with pneumonia caused by oral flora or anaerobes. In immunocompromised patients, the spectrum of possible pathogens also broadens to include fungi and parasites as well as less common bacterial and viral pathogens. (See "Epidemiology of pulmonary infections in immunocompromised patients" and "Approach to the immunocompromised patient with fever and pulmonary infiltrates" .)

While the list above details some of most common causes of CAP, >100 bacterial, viral, fungal, and parasitic causes have been reported. (See "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults", section on 'Microbiology' .)

Important trends  —  Both the distribution of pathogens that cause CAP and our knowledge of these pathogens are evolving. Key observations that have changed our understanding of CAP and influenced our approach to management include:

● Decline in S. pneumoniae incidence – Although S. pneumoniae (pneumococcus) is the most commonly detected bacterial cause of CAP in most studies, the overall incidence of pneumococcal pneumonia is decreasing. This is in part due to widespread use of pneumococcal vaccination, which results in both a decline in the individual rates of pneumococcal pneumonia and herd immunity in the population. (See "Pneumococcal pneumonia in patients requiring hospitalization", section on 'Prevalence' .)

Because pneumococcal vaccination rates vary regionally, the prevalence of S. pneumoniae infection also varies. As an example, S. pneumoniae is estimated to cause approximately 30 percent of cases of CAP in Europe but only 10 to 15 percent in the United States, where the population pneumococcal vaccination rate is higher [ 8 ].

● The coronavirus disease 2019 (COVID-19) pandemic – SARS-CoV-2 is an important cause of CAP and is discussed in detail elsewhere. (See "COVID-19: Epidemiology, virology, and prevention" .)

● Increased recognition of other respiratory viruses – Respiratory viruses have been detected in approximately one-third of cases of CAP in adults when using molecular methods [ 8 ]. The extent to which respiratory viruses serve as single pathogens, cofactors in the development of bacterial CAP, or triggers for dysregulated host immune response has not been established.

● Low overall rate of pathogen detection – Despite extensive evaluation using molecular diagnostics and other microbiologic testing methods, a causal pathogen can be identified in only half of cases of CAP. This finding highlights that our understanding of CAP pathogenesis is incomplete. As molecular diagnostics become more advanced and use broadens, our knowledge is expected to grow.

● Discovery of the lung microbiome – Historically, the lung has been considered sterile. However, culture-independent techniques (ie, high throughput 16S ribosomal ribonucleic acid [rRNA] gene sequencing) have identified complex and diverse communities of microbes that reside within the alveoli [ 19-21 ]. This finding suggests that resident alveolar microbes play a role in the development of pneumonia, either by modulating the host immune response to infecting pathogens or through direct overgrowth of specific pathogens within the alveolar microbiome. (See 'Pathogenesis' below.)

Antimicrobial resistance  —  Knowledge of antimicrobial resistance patterns and risk factors for infection with antimicrobial-resistant pathogens help inform the selection of antibiotics for empiric CAP treatment ( table 4 ).

● S. pneumoniae may be resistant to one or more antibiotics commonly used for the empiric treatment of CAP.

• Macrolide resistance rates vary regionally but are generally high (>25 percent) in the United States, Asia, and southern Europe. Resistance rates tend to be lower in northern Europe. (See "Resistance of Streptococcus pneumoniae to the macrolides, azalides, and lincosamides" .)

• Estimates of doxycycline resistance are less certain and vary substantially worldwide. In the United States, rates tend to be less than 20 percent but may be rising. (See "Resistance of Streptococcus pneumoniae to the fluoroquinolones, doxycycline, and trimethoprim-sulfamethoxazole" .)

• Beta-lactam resistance rates also vary regionally but to a lesser extent than macrolide and doxycycline resistance. In the United States, <20 percent of isolates are resistant to penicillin and <1 percent to cephalosporins. (See "Resistance of Streptococcus pneumoniae to beta-lactam antibiotics" .)

• Fluoroquinolone resistance tends to be <2 percent in the United States but varies regionally and with specific risk factors such as recent antibiotic use or hospitalization. (See "Resistance of Streptococcus pneumoniae to the fluoroquinolones, doxycycline, and trimethoprim-sulfamethoxazole" .)

Because resistance rates vary even at local levels, clinicians should refer to local antibiograms to guide antibiotic selection when available. General epidemiologic data can be obtained through sources such as the OneHealthTrust (formerly the Center for Disease Dynamics, Economics & Policy [CDDEP]).

● Methicillin-resistant S. aureus (MRSA) is an uncommon cause of CAP. Risk factors for MRSA have two patterns: health care associated and community acquired. The strongest risk factors for MRSA pneumonia include known MRSA colonization or prior MRSA infection, particularly involving the respiratory tract. Gram-positive cocci on sputum Gram stain are also predictive of MRSA infection. Other factors that should raise suspicion for MRSA infection include recent antibiotic use (particularly receipt of intravenous antibiotics within the past three months), recent influenza-like illness, the presence of empyema, necrotizing/cavitary pneumonia, and immunosuppression ( table 4 ).

In contrast with health care-associated MRSA, community-acquired MRSA (CA-MRSA) infections tend to occur in younger healthy persons [ 22 ]. Risk factors for CA-MRSA infection include a history of MRSA skin lesions, participation in contact sports, injection drug use, crowded living conditions, and men who have sex with men. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Epidemiology" .)

CAP caused by CA-MRSA can be severe and is associated with necrotizing and/or cavitary pneumonia, empyema, gross hemoptysis, septic shock, and respiratory failure. These features may be attributable to infection with toxin-producing CA-MRSA strains. In the United States, these strains tend to be methicillin resistant and belong to the USA300 clone. (See "Methicillin-resistant Staphylococcus aureus (MRSA): Microbiology and laboratory detection" .)

● Pseudomonas is also an uncommon cause of CAP and tends to occur more frequently in patients with known colonization or prior infection with Pseudomonas spp, recent hospitalization or antibiotic use, underlying structural lung disease (eg, cystic fibrosis or advanced chronic obstructive pulmonary disease [bronchiectasis]), and immunosuppression. Antibiotic resistance is common among pseudomonal strains, and empiric therapy with more than one agent that targets Pseudomonas is warranted for at-risk patients with moderate to severe CAP ( table 4 ). (See "Pseudomonas aeruginosa pneumonia" and 'Inpatient antibiotic therapy' below.)

PATHOGENESIS  —  Community-acquired pneumonia (CAP) pathogenesis Figure 3 Traditionally, CAP has been viewed as an infection of the lung parenchyma, primarily caused by bacterial or viral respiratory pathogens. In this model, respiratory pathogens are transmitted from person to person via droplets or, less commonly, via aerosol inhalation (eg, as with Legionella or Coxiella species). Following inhalation, the pathogen colonizes the nasopharynx and then reaches the lung alveoli via microaspiration. When the inoculum size is sufficient and/or host immune defenses are impaired, infection results. Replication of the pathogen, the production of virulence factors, and the host immune response lead to inflammation and damage of the lung parenchyma, resulting in pneumonia ( figure 3 ).

With the identification of the lung microbiome, that model has changed [ 19-21 ]. While the pathogenesis of pneumonia may still involve the introduction of respiratory pathogens into the alveoli, the infecting pathogen likely has to compete with resident microbes to replicate. In addition, resident microbes may also influence or modulate the host immune response to the infecting pathogen. If this is correct, an altered alveolar microbiome (alveolar dysbiosis) may be a predisposing factor for the development of pneumonia.

In some cases, CAP might also arise from uncontrolled replication of microbes that normally reside in the alveoli. The alveolar microbiome is similar to oral flora and is primarily comprised of anaerobic bacteria (eg, Prevotella and Veillonella ) and microaerophilic streptococci [ 19-21 ]. Hypothetically, exogenous insults such as a viral infection or smoke exposure might alter the composition of the alveolar microbiome and trigger overgrowth of certain microbes. Because organisms that compose the alveolar microbiome typically cannot be cultivated using standard cultures, this hypothesis might explain the low rate of pathogen detection among patients with CAP.

In any scenario, the host immune response to microbial replication within the alveoli plays an important role in determining disease severity. For some patients, a local inflammatory response within the lung predominates and may be sufficient for controlling infection. In others, a systemic response is necessary to control infection and to prevent spread or complications, such as bacteremia. In a minority, the systemic response can become dysregulated, leading to tissue injury, sepsis, acute respiratory distress syndrome, and/or multiorgan dysfunction.

The pathogenesis of CAP is discussed in greater detail separately. (See "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults" .)

CLINICAL PRESENTATION  —  The clinical presentation of CAP varies widely, ranging from mild pneumonia characterized by fever, cough, and shortness of breath to severe pneumonia characterized by sepsis and respiratory distress. Symptom severity is directly related to the intensity of the local and systemic immune response in each patient.

● Pulmonary signs and symptoms – Cough (with or without sputum production), dyspnea, and pleuritic chest pain are among the most common symptoms associated with CAP. Signs of pneumonia on physical examination include tachypnea, increased work of breathing, and adventitious breath sounds, including rales/crackles and rhonchi. Tactile fremitus, egophony, and dullness to percussion also suggest pneumonia. These signs and symptoms result from the accumulation of white blood cells (WBCs), fluid, and proteins in the alveolar space. Hypoxemia can result from the subsequent impairment of alveolar gas exchange. On chest radiograph, accumulation of WBCs and fluid within the alveoli appears as pulmonary opacities ( image 1A-B ).

● Systemic signs and symptoms – The great majority of patients with CAP present with fever. Other systemic symptoms such as chills, fatigue, malaise, chest pain (which may be pleuritic), and anorexia are also common. Tachycardia, leukocytosis with a leftward shift, or leukopenia are also findings that are mediated by the systemic inflammatory response. Inflammatory markers, such as the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and procalcitonin may rise, though the latter is largely specific to bacterial infections. CAP is also the leading cause of sepsis; thus, the initial presentation may be characterized by hypotension, altered mental status, and other signs of organ dysfunction such as renal dysfunction, liver dysfunction, and/or thrombocytopenia [ 23 ].

Although certain signs and symptom such as fever, cough, tachycardia, and rales are common among patients with CAP, these features are ultimately nonspecific and are shared among many respiratory disorders (see 'Differential diagnosis' below). No individual symptom or constellation of symptoms is adequate for diagnosis without chest imaging. For example, the positive predictive value of the combination of fever, tachycardia, rales, and hypoxia (oxygen saturation <95 percent) among patients with respiratory complaints presenting to primary care was <60 percent when chest radiograph was used as a reference standard [ 24 ].

Signs and symptoms of pneumonia can also be subtle in patients with advanced age and/or impaired immune systems, and a higher degree of suspicion may be needed to make the diagnosis. As examples, older patients may present with mental status changes but lack fever or leukocytosis [ 25 ]. In immunocompromised patients, pulmonary infiltrates may not be detectable on chest radiographs but can be visualized with computed tomography.

The clinical and diagnostic features of CAP and sepsis are discussed in detail separately. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults" and "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis", section on 'Clinical presentation' .)

Making the diagnosis  —  The diagnosis of CAP generally requires the demonstration of an infiltrate on chest imaging in a patient with a clinically compatible syndrome (eg, fever, dyspnea, cough, and sputum production) [ 26 ].

● For most patients with suspected CAP, we obtain posteroanterior and lateral chest radiographs. Radiographic findings consistent with the diagnosis of CAP include lobar consolidations ( image 1C ), interstitial infiltrates ( image 1D-E ), and/or cavitations ( image 2 ). Although certain radiographic features suggest certain causes of pneumonia (eg, lobar consolidations suggest infection with typical bacterial pathogens), radiographic appearance alone cannot reliably differentiate among etiologies.

● For selected patients in whom CAP is suspected based on clinical features despite a negative chest radiograph, we obtain computed tomography (CT) of the chest. These patients include immunocompromised patients, who may not mount strong inflammatory responses and thus have negative chest radiographs, as well as patients with known exposures to epidemic pathogens that cause pneumonia (eg, Legionella ). Because there is no direct evidence to suggest that CT scanning improves outcomes for most patients and cost is high, we do not routinely obtain CT scans when evaluating patients for CAP.

The combination of a compatible clinical syndrome and imaging findings consistent with pneumonia are sufficient to establish an initial clinical diagnosis of CAP. However, this combination of findings is nonspecific and is shared among many cardiopulmonary disorders. Thus, remaining attentive to the possibility of an alternate diagnosis as a patient's course evolves is important to care. (See 'Differential diagnosis' below.)

Defining severity and site of care  —  For patients with a working diagnosis of CAP, the next steps in management are defining the severity of illness and determining the most appropriate site of care. Determining the severity of illness is based on clinical judgement and can be supplemented by use of severity scores ( algorithm 1 ).

The most commonly used severity scores are the Pneumonia Severity Index (PSI) and CURB-65 [ 27,28 ]. We generally prefer the PSI, also known as the PORT score ( calculator 1 ), because it is the most accurate and its safety and effectiveness in guiding clinical decision-making have been validated [ 29-32 ]. However, the CURB-65 score is a reasonable alternative and is preferred by many clinicians because it is easier to use ( calculator 2 ).

The three levels of severity (mild, moderate, and severe) generally correspond to three levels of care:

● Ambulatory care – Most patients who are otherwise healthy with normal vital signs (apart from fever) and no concern for complication are considered to have mild pneumonia and can be managed in the ambulatory setting. These patients typically have PSI scores of I to II and CURB-65 scores of 0 (or a CURB-65 score of 1 if age >65 years).

● Hospital admission – Patients who have peripheral oxygen saturations <92 percent on room air (and a significant change from baseline) should be hospitalized. In addition, patients with PSI scores of ≥III and CURB-65 scores ≥1 (or CURB-65 score ≥2 if age >65 years) should also generally be hospitalized.

Because patients with early signs of sepsis, rapidly progressive illness, or suspected infections with aggressive pathogens are not well represented in severity scoring systems, these patients may also warrant hospitalization in order to closely monitor the response to treatment.

Practical concerns that may warrant hospital admission include an inability to take oral medications, cognitive or functional impairment, or other social issues that could impair medication adherence or ability to return to care for clinical worsening (eg, substance abuse, homelessness, or residence far from a medical facility).

● Intensive care unit (ICU) admission – Patients who meet either of the following major criteria have severe CAP and should be admitted to the ICU [ 26 ]:

• Respiratory failure requiring mechanical ventilation

• Sepsis requiring vasopressor support

Recognizing these two criteria for ICU admission is relatively straightforward. The challenge is to identify patients with severe CAP who have progressed to sepsis before the development of organ failure. For these patients, early ICU admission and administration of appropriate antibiotics improve outcomes. To help identify patients with severe CAP before development of organ failure, the American Thoracic Society (ATS) and the Infectious Diseases Society of America (IDSA) suggest minor criteria [ 1,26 ].

The presence of three of these criteria warrants ICU admission:

• Altered mental status

• Hypotension requiring fluid support

• Temperature <36°C (96.8°F)

• Respiratory rate ≥30 breaths/minute

• Arterial oxygen tension to fraction of inspired oxygen (PaO 2 /FiO 2 ) ratio ≤250

• Blood urea nitrogen (BUN) ≥20 mg/dL (7 mmol/L)

• Leukocyte count <4000 cells/microL

• Platelet count <100,000/microL

• Multilobar infiltrates

Although several other scores for identifying patients with severe CAP and/or ICU admission have been developed, we generally use the ATS/IDSA major and minor criteria because they are well validated [ 33-35 ].

Detailed discussion on assessing severity and determining the site of care in patients with CAP is provided separately. (See "Community-acquired pneumonia in adults: Assessing severity and determining the appropriate site of care" .) (Related Pathway(s): Community-acquired pneumonia: Determining the appropriate site of care for adults .)

Triage of patients with known or suspected COVID-19 is also discussed elsewhere. (See "COVID-19: Evaluation of adults with acute illness in the outpatient setting", section on 'Disposition' .)

Microbiologic testing  —  The benefit of obtaining a microbiologic diagnosis should be balanced against the time and cost associated with an extensive evaluation in each patient.

Generally, we take a tiered approach to microbiologic evaluation based on CAP severity and the site of care ( table 5 ):

● Outpatients − For most patients with mild CAP being treated in the ambulatory setting, microbiologic testing is not needed (apart from testing for SARS-CoV-2 during the pandemic). Empiric antibiotic therapy is generally successful, and knowledge of the infecting pathogen does not usually improve outcomes.

● Patients with moderate CAP admitted to the general medicine ward − For most patients with moderate CAP admitted to the general medical ward, we obtain the following:

• Blood cultures

• Sputum Gram stain and culture

• Urinary antigen testing for S. pneumoniae

• Testing for Legionella spp (polymerase chain reaction [PCR] when available, urinary antigen test as an alternate)

• SARS-CoV-2 testing

During the pandemic, we test all patients for COVID-19. During respiratory virus season (eg, late fall to early spring in the northern hemisphere), we also test for other respiratory viruses (eg, influenza, adenovirus, parainfluenza, respiratory syncytial virus, and human metapneumovirus). When testing for influenza, PCR is preferred over rapid antigen testing. (See "Seasonal influenza in adults: Clinical manifestations and diagnosis" .)

For these patients, making a microbiologic diagnosis allows for directed therapy, which helps limit antibiotic overuse, prevent antimicrobial resistance, and reduce unnecessary complications, such as Clostridioides difficile infections.

● Patients with severe CAP (including ICU admission) − For most hospitalized patients with severe CAP, including those admitted to the ICU, we send blood cultures, sputum cultures, urinary streptococcal antigen, and Legionella testing. In addition, we obtain bronchoscopic specimens for microbiologic testing when feasible, weighing the benefits of obtaining a microbiologic diagnosis against the risks of the procedure (eg, need for intubation, bleeding, bronchospasm, pneumothorax) on a case-by-case basis. When pursuing bronchoscopy, we usually send specimens for aerobic culture, Legionella culture, fungal stain and culture, and testing for respiratory viruses.

The type of viral diagnostic tests used (eg, PCR, serology, culture) vary among institutions. In some cases, multiplex PCR panels that test for a wide array of viral and bacterial pathogens are used. While we generally favor using these tests for patients with severe pneumonia, we interpret results with caution as most multiplex assays have not been approved for use on lower respiratory tract specimens. In particular, the detection of single viral pathogen does not confirm the diagnosis of viral pneumonia because viruses can serve as cofactors in the pathogenesis of bacterial CAP or can be harbored asymptomatically.

In all cases, we modify this approach based on epidemiologic exposures, patient risk factors, and clinical features regardless of CAP severity or treatment setting ( table 3 ). As examples:

● For patients with known or probable exposures to epidemic pathogens such as Legionella or epidemic coronaviruses, we broaden our evaluation to include tests for these pathogens. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults", section on 'Important pathogens' .)

● For patients with cavitary pneumonia, we may include testing for tuberculosis, fungal pathogens, and Nocardia .

● For immunocompromised patients, we broaden our differential to include opportunistic pathogens such as Pneumocystis jirovecii , fungal pathogens, parasites, and less common viral pathogens such as cytomegalovirus. The approach to diagnostic testing varies based on the type and degree of immunosuppression and other patient-specific factors. (See "Approach to the immunocompromised patient with fever and pulmonary infiltrates" and "Epidemiology of pulmonary infections in immunocompromised patients" .)

When defining the scope of our microbiologic evaluation, we also take the certainty of the diagnosis of CAP into consideration. Because a substantial portion of patients hospitalized with an initial clinical diagnosis of CAP are ultimately found to have alternate diagnoses [ 17 ], pursuing a comprehensive microbiologic evaluation can help reach the final diagnosis (eg, blood cultures obtained as part of the evaluation for CAP may help lead to a final diagnosis of endocarditis).

Detailed discussion on the microbiologic evaluation of CAP is provided separately. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults" and "Sputum cultures for the evaluation of bacterial pneumonia" .)

The diagnosis of COVID-19 during the pandemic is also discussed in detail elsewhere. (See "COVID-19: Diagnosis" .)

DIFFERENTIAL DIAGNOSIS  —  CAP is a common working diagnosis and is frequently on the differential diagnosis of patients presenting with a pulmonary infiltrate and cough, patients with respiratory tract infections, and patients with sepsis. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults", section on 'Differential diagnosis' .)

Noninfectious illnesses that mimic CAP or co-occur with CAP and present with pulmonary infiltrate and cough include:

• Congestive heart failure with pulmonary edema

• Pulmonary embolism

• Pulmonary hemorrhage

• Atelectasis

• Aspiration or chemical pneumonitis

• Drug reactions

• Lung cancer

• Collagen vascular diseases

• Vasculitis

• Acute exacerbation of bronchiectasis

• Interstitial lung diseases (eg, sarcoidosis, asbestosis, hypersensitivity pneumonitis, cryptogenic organizing pneumonia)

For patients with an initial clinical diagnosis of CAP who have rapidly resolving pulmonary infiltrates, alternate diagnoses should be investigated. Pulmonary infiltrates in CAP are primarily caused by the accumulation of white blood cells (WBCs) in the alveolar space and typically take weeks to resolve. A pulmonary infiltrate that resolves in one or two days may be caused by accumulation of fluid in the alveoli (ie, pulmonary edema) or a collapse of the alveoli (ie, atelectasis) but not due to accumulation of WBCs.

Respiratory illnesses that mimic CAP or co-occur with CAP include:

• Acute exacerbations of chronic obstructive pulmonary disease

• Influenza and other respiratory viral infections

• Acute bronchitis ( figure 4 )

• Asthma exacerbations

Febrile illness and/or sepsis can also be the presenting syndrome in patients with CAP; other common causes of these syndromes include urinary tract infections, intraabdominal infections, and endocarditis.

TREATMENT  —  For most patients with CAP and excluding COVID-19, the etiology is not known at the time of diagnosis, and antibiotic treatment is empiric, targeting the most likely pathogens. The pathogens most likely to cause CAP vary with severity of illness, local epidemiology, and patient risk factors for infection with drug-resistant organisms.

As an example, for most patients with mild CAP who are otherwise healthy and treated in the ambulatory setting, the range of potential pathogens is limited. By contrast, for patients with CAP severe enough to require hospitalization, potential pathogens are more diverse, and the initial treatment regimens are often broader. (Related Pathway(s): Community-acquired pneumonia: Empiric antibiotic selection for adults in the outpatient setting and Community-acquired pneumonia: Empiric antibiotic selection for adults admitted to a general medical ward and Community-acquired pneumonia: Empiric antibiotic selection for adults admitted to the intensive care unit .)

The management of COVID-19 is discussed in detail elsewhere. (See "COVID-19: Management in hospitalized adults" and "COVID-19: Management of adults with acute illness in the outpatient setting" .)

Outpatient antibiotic therapy  —  For all patients with CAP, empiric regimens are designed to target S. pneumoniae (the most common and virulent bacterial CAP pathogen) and atypical pathogens. Coverage is expanded for outpatients with comorbidities, smoking, and recent antibiotic use to include or better treat beta-lactamase-producing H. influenzae , M. catarrhalis , and methicillin-susceptible S. aureus . For those with structural lung disease, we further expand coverage to include Enterobacteriaceae, such as E. coli and Klebsiella spp ( algorithm 2 ).

Selection of the initial regimen depends on the adverse effect profiles of available agents, potential drug interactions, patient allergies, and other patient-specific factors.

● For most patients aged <65 years who are otherwise healthy and have not recently used antibiotics, we typically use oral amoxicillin (1 g three times daily) plus a macrolide (eg, azithromycin or clarithromycin ) or doxycycline . Generally, we prefer to use a macrolide over doxycycline.

This approach differs from the American Thoracic Society (ATS)/Infectious Diseases Society of America (IDSA), which recommend monotherapy with amoxicillin as first line and monotherapy with either doxycycline or a macrolide (if local resistance rates are <25 percent [eg, not in the United States]) as alternatives for this population [ 26 ]. The rationale for each approach is discussed separately. (See "Treatment of community-acquired pneumonia in adults in the outpatient setting", section on 'Empiric antibiotic treatment' .)

● For patients who have major comorbidities (eg, chronic heart, lung, kidney, or liver disease, diabetes mellitus, alcohol dependence, or immunosuppression), who are smokers, and/or who have used antibiotics within the past three months, we suggest oral amoxicillin-clavulanate (875 mg twice daily or extended release 2 g twice daily) plus either a macrolide (preferred) or doxycycline .

Alternatives to amoxicillin-based regimens include combination therapy with a cephalosporin plus a macrolide or doxycycline or monotherapy with lefamulin .

● For patients who can use cephalosporins, we use a third-generation cephalosporin (eg, cefpodoxime ) plus either a macrolide or doxycycline .

● For patients who cannot use any beta-lactam, we select a respiratory fluoroquinolone (eg, levofloxacin , moxifloxacin , gemifloxacin ) or lefamulin . For those with structural lung disease, we prefer a respiratory fluoroquinolone because its spectrum of activity includes Enterobacteriaceae.

In the absence of hepatic impairment or drug interactions, lefamulin is a potential alternative to fluoroquinolones for most others. However, clinical experience with this agent is limited. Use should be avoided in patients with moderate to severe hepatic dysfunction, known long QT syndrome, or in those taking QT-prolonging agents, pregnant and breastfeeding women, and women with reproductive potential not using contraception. There are drug interactions with CYP3A4 and P-gp inducers and substrates; in addition, lefamulin tablets are contraindicated with QT-prolonging CYP3A4 substrates. Refer to the drug interactions program included within UpToDate.  

Omadacycline is another newer agent that is active against most CAP pathogens, including Enterobacteriaceae. It is a potential alternative for patients who cannot tolerate beta-lactams (or other agents) and want to avoid fluoroquinolones. (See "Treatment of community-acquired pneumonia in adults who require hospitalization", section on 'New antimicrobial agents' .)

Modifications to these regimens may be needed for antibiotic allergy, drug interactions, specific exposures, and other patient-specific factors. In particular, during influenza season, patients at high risk for poor outcomes from influenza may warrant antiviral therapy ( table 6 ).

We treat most patients for five days. However, we generally ensure that all patients are improving on therapy and are afebrile for at least 48 hours before stopping antibiotics. In general, extending the treatment course beyond seven days does not add benefit. Studies supporting this approach are discussed separately. (See "Treatment of community-acquired pneumonia in adults in the outpatient setting", section on 'Duration of therapy' .)

Detailed discussion on the treatment of CAP in the outpatient setting, including antibiotic efficacy data, is provided separately. (See "Treatment of community-acquired pneumonia in adults in the outpatient setting" .) (Related Pathway(s): Community-acquired pneumonia: Empiric antibiotic selection for adults in the outpatient setting .)

Inpatient antibiotic therapy

General medical ward  —  For patients with CAP admitted to the medical ward, empiric antibiotic regimens are designed to treat S. aureus , gram-negative enteric bacilli (eg, Klebsiella pneumoniae ) in addition to typical pathogens (eg, S. pneumoniae , H. influenzae , and M. catarrhalis ) and atypical pathogens (eg, Legionella pneumophilia , M. pneumoniae , and C. pneumoniae ).

We generally start antibiotic therapy as soon as we are confident that CAP is the appropriate working diagnosis and, ideally, within four hours of presentation. Delays in appropriate antibiotic treatment that exceed four hours have been associated with increased mortality [ 36 ].

The key factors in selecting an initial regimen for hospitalized patients with CAP are risk of infection with Pseudomonas and/or methicillin-resistant S. aureus (MRSA). The strongest risk factors for MRSA or Pseudomonas infection are known colonization or prior infection with these organisms, particularly from a respiratory tract specimen. Recent hospitalization (ie, within the past three months) with receipt of intravenous (IV) antibiotics is also a risk factor, particularly for pseudomonal infection. Suspicion for these pathogens should otherwise be based on local prevalence (when known), other patient-specific risk factors, and the overall clinical assessment ( algorithm 3 and table 4 ):

● For patients without suspicion for MRSA or Pseudomonas , we generally use one of two regimens: combination therapy with a beta-lactam plus a macrolide or monotherapy with a respiratory fluoroquinolone [ 26 ]. Because these two regimens have similar clinical efficacy, we select among them based on other factors (eg, antibiotic allergy, drug interactions). For patients who are unable to use either a macrolide or a fluoroquinolone, we use a beta-lactam plus doxycycline .

● For patients with known colonization or prior infection with Pseudomonas, recent hospitalization with IV antibiotic use, or other strong suspicion for pseudomonal infection , we typically use combination therapy with both an antipseudomonal beta-lactam (eg, piperacillin-tazobactam , cefepime , ceftazidime , meropenem , or imipenem ) plus an antipseudomonal fluoroquinolone (eg, ciprofloxacin or levofloxacin ). The selection of empiric regimens should also be informed by the susceptibility pattern for prior isolates.

● For patients with known colonization or prior infection with MRSA or other strong suspicion for MRSA infection , we add an agent with anti-MRSA activity, such as vancomycin or linezolid , to either of the above regimens. We generally prefer linezolid over vancomycin when community-acquired MRSA is suspected (eg, a young, otherwise healthy patient who plays contact sports presenting with necrotizing pneumonia) because of linezolid's ability to inhibit bacterial toxin production [ 37 ]. Ceftaroline is a potential alternative for the treatment of MRSA pneumonia but is not US Food and Drug Administration approved. (See "Treatment of community-acquired pneumonia in adults who require hospitalization", section on 'Community-acquired MRSA' .)

Modifications to initial empiric regimens may be needed for antibiotic allergy, potential drug interactions, current epidemics, specific exposures, resistance patterns of known colonizing organisms or organisms isolated during prior infections, and other patient-specific factors. In particular, antiviral treatment (eg, oseltamivir ) should be given as soon as possible for any hospitalized patient with known or suspected influenza. (See "Seasonal influenza in nonpregnant adults: Treatment" .)

Detailed discussion about antibiotic therapy, including use of new agents (eg, lefamulin , omadacycline ) for patients hospitalized to a general medical ward is provided separately. (See "Treatment of community-acquired pneumonia in adults who require hospitalization" .) (Related Pathway(s): Community-acquired pneumonia: Empiric antibiotic selection for adults admitted to a general medical ward .)

ICU admission

Antibiotic selection  —  For patients with CAP admitted to the intensive care unit (ICU), our approach to antibiotic selection is similar to that used for patients admitted to the general medical ward. However, because of the severity of illness in this population, we do not use monotherapy ( algorithm 4 ). In addition, we start antibiotic therapy within one hour of presentation for patients who are critically ill.

The spectrum of activity of the empiric regimen should be broadened in patients with risk factors for Pseudomonas infection or MRSA infection ( table 4 ).

● For most patients without suspicion for MRSA or Pseudomonas , we treat with a beta-lactam (eg, ceftriaxone , cefotaxime , ceftaroline , ampicillin-sulbactam , ertapenem ) plus a macrolide (eg, azithromycin or clarithromycin ) or a beta-lactam plus a respiratory fluoroquinolone (eg, levofloxacin or moxifloxacin ) [ 26 ].

For patients with penicillin hypersensitivity reactions, we select an appropriate agent (eg, later-generation cephalosporin, carbapenem, or a beta-lactam alternative) based on the type and severity of reaction ( algorithm 5 ). For patients who cannot use any beta-lactam (ie, penicillins, cephalosporins, and carbapenems), we typically use combination therapy with a respiratory fluoroquinolone and aztreonam .

● For patients with known colonization or prior infection with MRSA, recent hospitalization with IV antibiotic use, or other strong suspicion for MRSA infection , we add an agent with anti-MRSA activity, such as vancomycin or linezolid , to either of the above regimens [ 26 ].

● For patients with known colonization or prior infection with Pseudomonas , recent hospitalization with IV antibiotic use, or other strong suspicion for pseudomonal infection , we typically use combination therapy with both an antipseudomonal beta-lactam (eg, piperacillin-tazobactam , cefepime , ceftazidime , meropenem , or imipenem ) plus an antipseudomonal fluoroquinolone (eg, ciprofloxacin or levofloxacin ) for empiric treatment [ 26 ].

For patients with penicillin hypersensitivity reactions, we select an appropriate agent based on the type and severity of penicillin reaction ( algorithm 5 ) and prior pseudomonal susceptibility testing.

Modifications to initial empiric regimens may be needed for antibiotic allergy, potential drug interactions, current epidemics, specific exposures, resistance patterns of colonizing bacteria or bacteria isolated during prior infections, and other patient-specific factors. In particular, antiviral treatment (eg, oseltamivir ) should be given as soon as possible for any hospitalized patient with known or suspected influenza. (See "Seasonal influenza in nonpregnant adults: Treatment" .)

Detailed discussion about antibiotic treatment for patients with CAP admitted to the ICU and patients with sepsis and/or respiratory failure are provided separately. (See "Treatment of community-acquired pneumonia in adults who require hospitalization", section on 'Intensive care unit' and "Evaluation and management of suspected sepsis and septic shock in adults" .) (Related Pathway(s): Community-acquired pneumonia: Empiric antibiotic selection for adults admitted to the intensive care unit .)

Adjunctive glucocorticoids  —  The role of adjunctive glucocorticoid treatment for CAP is evolving. The rationale for use is to reduce the inflammatory response to pneumonia, which may in turn reduce progression to lung injury, ARDS, and mortality. Based on randomized trials, the greatest benefit is for patients with impending respiratory failure or those requiring mechanical ventilation, particularly when glucocorticoids are given early in the course.

● For most immunocompetent patients with respiratory failure due to CAP who require invasive or non-invasive mechanical ventilation or with significant hypoxemia (ie, PaO2:FIO2 ratio <300 with an FiO 2 requirement of ≥50 percent and use of either high flow nasal cannula or a nonrebreathing mask), we suggest continuous infusion of hydrocortisone 200 mg daily for 4 to 7 days followed by a taper. Because mortality benefit appears to be greatest with early initiation, hydrocortisone should ideally be started as soon as possible. The decision to taper glucocorticoids at day 4 or 7 is based on clinical response.

● Because glucocorticoid use may impair the immune control of influenza, tuberculosis, and fungal pathogens, we avoid hydrocortisone use in patients with CAP caused by these pathogens or for patients with concurrent acute viral hepatitis or active herpes viral infection, which may also be worsened with glucocorticoid use.

● For immunocompromised patients, we weigh the risks and benefits of use on an individual basis.

● While we do not treat CAP with adjunctive glucocorticoids in most other circumstances, we do not withhold glucocorticoids when they are indicated for other reasons, including:

• Refractory septic shock (see "Glucocorticoid therapy in septic shock in adults" )

• Acute exacerbations of COPD (see "COPD exacerbations: Management", section on 'Glucocorticoids in moderate to severe exacerbations' )

• COVID-19 (see "COVID-19: Management in hospitalized adults", section on 'Dexamethasone and other glucocorticoids' )

Additional detail on the use of glucocorticoids for CAP and review of the evidence are discussed separately. (See "Treatment of community-acquired pneumonia in adults who require hospitalization", section on 'Adjunctive glucocorticoids' .)

Disposition  —  Once a patient with CAP is hospitalized, further management will be dictated by the patient's response to initial empiric therapy. Clinical response should be assessed during daily rounds. While various criteria have been proposed to assess clinical response [ 38-40 ], we generally look for subjective improvement in cough, sputum production, dyspnea, and chest pain. Objectively, we assess for resolution of fever and normalization of heart rate, respiratory rate, oxygenation, and white blood cell count. Generally, patients demonstrate some clinical improvement within 48 to 72 hours ( table 7 ).

Antibiotic de-escalation  —  For patients in whom a causative pathogen has been identified, we tailor therapy to target the pathogen [ 41 ]. If coverage for MRSA was added empirically, and MRSA was not identified as a pathogen nor on a screening nasal swab and the patient is improving, we typically discontinue the anti-MRSA agent (eg, vancomycin ). However, for the majority of patients hospitalized with CAP, a causative pathogen is not identified. For these patients, we continue empiric treatment for the duration of therapy, provided that the patient is improving. Intravenous antibiotic regimens can be transitioned to oral regimens with a similar spectrum activity as the patient improves ( algorithm 6 ) [ 42,43 ].

Duration of therapy  —  We generally determine the duration of therapy based on the patient's clinical response to therapy.

For all patients, we treat until the patient has been afebrile and clinically stable for at least 48 hours and for a minimum of five days. Patients with mild infection generally require five to seven days of therapy. Patients with severe infection or chronic comorbidities generally require 7 to 10 days of therapy. Extended courses may be needed for immunocompromised patients, patients with infections caused by certain pathogens (eg, P. aeruginosa) , or those with complications. (See "Treatment of community-acquired pneumonia in adults who require hospitalization", section on 'Duration of therapy' .)

In accord with the ATS/IDSA, we do not use procalcitonin to help determine whether to start antibiotics [ 26 ]. However, we sometimes use procalcitonin thresholds as an adjunct to clinical judgment to help guide antibiotic discontinuation in clinically stable patients. We generally obtain a level at the time of diagnosis and repeat the level every one to two days in patients who are clinically stable. We determine the need for continued antibiotic therapy based on clinical improvement and serial procalcitonin levels ( algorithm 7 ). (See "Procalcitonin use in lower respiratory tract infections" .)

Discharge  —  Hospital discharge is appropriate when the patient is clinically stable, can take oral medication, has no other active medical problems, and has a safe environment for continued care. Patients do not need to be kept overnight for observation following the switch to oral therapy. Early discharge based on clinical stability and criteria for switching to oral therapy is encouraged to reduce risk associated with prolonged hospital stays and unnecessary cost.

Immunocompromised patients  —  The spectrum of potential pathogens expands considerably in immunocompromised patients to include invasive fungal infections, less common viral infections (eg, cytomegalovirus), and parasitic infections (eg, toxoplasmosis) [ 44 ].

The risk for specific infections varies with the type and degree of immunosuppression and whether the patient is taking prophylactic antimicrobials. As examples, prolonged neutropenia, T cell immunosuppression, and use of tumor necrosis factor-alpha inhibitors predispose to invasive fungal infections (eg, aspergillosis, mucormycosis) as well as mycobacterial infections. Advanced human immunodeficiency virus (HIV) infection (eg, CD4 cell count <200 cells/microL), prolonged glucocorticoid use (particularly when used with certain chemotherapeutics), and lymphopenia each should raise suspicion for pneumocystis pneumonia. Multiple infections may occur concurrently in this population, and the likelihood of disseminated infection is greater. Because signs and symptoms of infection can be subtle and nonspecific in immunocompromised patients, diagnosis can be challenging and invasive procedures are often required for microbiologic diagnosis. Broad-spectrum empiric therapy may be needed prior to obtaining a specific microbiologic diagnosis [ 45 ].

Because management is complex, drug interactions are common, adjustments in immunosuppressive regimens may be needed, and empiric treatment options (eg, amphotericin B) can be associated with significant toxicity, we generally involve a multidisciplinary team of specialists when caring for immunocompromised patients with pneumonia. (See "Epidemiology of pulmonary infections in immunocompromised patients" and "Approach to the immunocompromised patient with fever and pulmonary infiltrates" and "Tumor necrosis factor-alpha inhibitors: Bacterial, viral, and fungal infections" .)

FOLLOW-UP IMAGING  —  Follow-up imaging for immunocompetent adults who have recovered from community-acquired pneumonia Algorithm 8 Most patients with clinical resolution after treatment do not require a follow-up chest radiograph, as radiographic response lags behind clinical response. However, follow-up clinic visits are good opportunities to review the patient's risk for lung cancer based on age, smoking history, and recent imaging findings ( algorithm 8 ).

This approach is similar to that outlined by the ATS/IDSA, which recommend not obtaining a follow-up chest radiograph in patients whose symptoms have resolved within five to seven days [ 26 ]. (See "Treatment of community-acquired pneumonia in adults who require hospitalization", section on 'Follow-up chest radiograph' .)

COMPLICATIONS AND PROGNOSIS  —  While most patients with CAP will recover with appropriate antibiotic treatment, some will progress and/or develop complications despite appropriate therapy (ie, clinical failure) and some will remain symptomatic (ie, nonresolving pneumonia).

Clinical failure  —  Clear indicators of clinical failure include progression to sepsis and/or respiratory failure despite appropriate antibiotic treatment and respiratory support. Other indicators include an increase in subjective symptoms (eg, cough, dyspnea) usually in combination with objective criteria (eg, decline in oxygenation, persistent fever, or rising white blood cell). Various criteria have been proposed to define clinical failure but none widely adopted [ 46-48 ].

Reasons for clinical failure generally fall into these categories:

● Progression of the initial infection – For some patients, CAP can lead to overwhelming infection despite appropriate antibiotic treatment. In some, this indicates a dysregulated host immune response. In others, this may indicate that the infection has spread beyond the pulmonary parenchyma (eg, empyema, lung abscess, bacteremia, endocarditis).

Other possibilities include infection with a drug-resistant pathogen or an unusual pathogen not covered by the initial empiric antibiotic regimen. Alternatively, failure to respond to treatment may signify the presence of an immunodeficiency (eg, new diagnosis of HIV infection).

● Development of comorbid complications – Comorbid complications may be infectious or noninfectious. Nosocomial infections, particularly hospital-acquired pneumonia (HAP), are common causes of clinical failure. In addition to HAP, others include catheter-related bloodstream infections, urinary tract infections, and C. difficile infection [ 49 ].

Cardiovascular events are also common complications and include acute myocardial infarction, cardiac arrhythmias, congestive heart failure, pulmonary embolism, and stroke [ 50-52 ]. Older age, preexisting cardiovascular disease, severe pneumonia, and infection with certain pathogens (ie, S. pneumoniae and influenza) have each been associated with increased risk of cardiovascular events [ 50,53-55 ]. Recognition that cardiovascular events and other systemic complications can occur during the acute phase of CAP is also changing our view of CAP from an acute pulmonary process to an acute systemic disease. (See "Morbidity and mortality associated with community-acquired pneumonia in adults", section on 'Cardiac complications' .)

Because of these possibilities, we generally broaden our initial antibiotic regimen for patients who are progressing despite appropriate empiric treatment and evaluate for alternate diagnoses, less common or drug-resistant pathogens, and/or infectious and cardiovascular complications. (See 'Differential diagnosis' above and "Morbidity and mortality associated with community-acquired pneumonia in adults" .)

Nonresolving CAP  —  For some patients, initial symptoms will neither progress nor improve with at least seven days of appropriate empiric antibiotic treatment. We generally characterize these patients as having nonresolving pneumonia. Potential causes of nonresolving CAP include:

● Delayed clinical response – For some patients, particularly those with multiple comorbidities, severe pneumonia, bacteremia, and infection with certain pathogens (eg, S. pneumoniae ), treatment response may be slow. Eight or nine days of treatment may be needed before clinical improvement is evident.

● Loculated infection – Patients with complications such as lung abscess, empyema, or other closed space infections may fail to improve clinically despite appropriate antibiotic selection. Such infections may require drainage and/or prolonged antibiotic treatment. (See "Lung abscess in adults" and "Epidemiology, clinical presentation, and diagnostic evaluation of parapneumonic effusion and empyema in adults" .)

● Bronchial obstruction – Bronchial obstruction (eg, by a tumor) can cause a postobstructive pneumonia that may fail to respond or slowly respond to standard empiric antibiotic regimens for CAP.

● Pathogens that cause subacute/chronic CAP – Mycobacterium tuberculosis , nontuberculous mycobacteria (eg, Mycobacterium kansasii ), fungi (eg, Histoplasma capsulatum , Blastomyces dermatitidis ), or less common bacteria (eg, Nocardia spp, Actinomyces israelii ) can cause subacute or chronic pneumonia that may fail to respond or may incompletely respond to standard empiric antibiotic regimens for CAP.

● Incorrect initial diagnosis – Failure to improve despite seven days of treatment also raises the possibility of an alternate diagnosis (eg, malignancy or inflammatory lung disease). (See 'Differential diagnosis' above.)

Once a patient is characterized as having nonresolving CAP, a complete new physical examination, laboratory evaluation, imaging studies, and microbiologic workup will be necessary to define the etiology of nonresolving CAP [ 49 ]. Initiation of workup for nonresolving CAP should not be automatically associated with a change in initial empiric antibiotic therapy. (See "Nonresolving pneumonia" .)

Long-term complications and mortality  —  Although the majority of patient with CAP recover without complications, CAP is a severe illness and among the leading causes of mortality worldwide. Mortality can be directly attributable to CAP (eg, overwhelming sepsis or respiratory failure) or can result indirectly from cardiovascular events or other comorbid complications (eg, advanced chronic obstructive pulmonary disease [COPD]) [ 56 ].

Long-term complications resulting from pneumonia are increasingly recognized and there is a shift in the medical community to define pneumonia as a systemic illness that can lead to chronic disease [ 57 ]. While the precise incidence of long-term complications is not known, the more common long-term sequelae involve the respiratory tract and cardiovascular system [ 58 ].

In the United States, pneumonia (combined with influenza) is among the top 10 most common causes of death [ 5 ]. Thirty-day mortality rates vary with disease severity, ranging from less than 1 percent in ambulatory patients to approximately 20 to 25 percent in patients with severe CAP. In addition to disease severity, older age, comorbidities (eg, COPD, diabetes mellitus, cardiovascular disease), infection with certain pathogens (eg, S. pneumoniae ), and acute cardiac complications are each associated with increased short-term mortality [ 50,59,60 ].

CAP is also associated with increased long-term mortality [ 7,61-63 ]. In one population-based study evaluating 7449 patients hospitalized with CAP, mortality rates were 6.5 percent during hospitalization, 13 percent 30 days after hospitalization, 23 percent at six months after hospitalization, and 31 percent at one year after hospitalization [ 7 ]. During the same study year, an estimated 1,581,860 patients were hospitalized in the United States. Extrapolating mortality data to these patients, the number of deaths in the United States population will be 102,821 during hospitalization, 205,642 at 30 days, 370,156 at six months, and 484,050 at one year [ 7 ]. Causes of long-term mortality are primarily related to comorbidities and include malignancy, COPD, and cardiovascular disease [ 56 ].

Data associating CAP with long-term mortality indicate that CAP is not only a common cause of acute morbidity and mortality but also a disease with important chronic health outcomes.

PREVENTION  —  The three primary pillars for the prevention of CAP are [ 64-66 ]:

● Smoking cessation (when appropriate)

● Influenza vaccination for all patients

● Pneumococcal vaccination for at-risk patients

Each is discussed in detail separately. (See "Overview of smoking cessation management in adults" and "Seasonal influenza vaccination in adults" and "Pneumococcal vaccination in adults" .)

SOCIETY GUIDELINE LINKS  —  Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Community-acquired pneumonia in adults" .)

INFORMATION FOR PATIENTS  —  UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5 th to 6 th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10 th to 12 th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

● Basics topic (see "Patient education: Pneumonia in adults (The Basics)" )

● Beyond the Basics topic (see "Patient education: Pneumonia in adults (Beyond the Basics)" )

SUMMARY AND RECOMMENDATIONS

● Background – Community-acquired pneumonia (CAP) is a leading cause of morbidity and mortality worldwide. (See 'Incidence' above.)

● Risk factors – Risk factors include age ≥65 years, chronic comorbidities, concurrent or antecedent respiratory viral infections, impaired airway protection, smoking, alcohol abuse, and other lifestyle factors (eg, crowded living conditions). (See 'Risk factors' above.)

● Microbiology – The most commonly identified causes of CAP include respiratory viruses (particularly severe acute respiratory syndrome coronavirus 2 during the pandemic), typical bacteria (eg, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis ) and atypical bacteria (eg, Legionella spp, Mycoplasma pneumoniae, Chlamydia pneumoniae ). Pseudomonas and methicillin-resistant Staphylococcus aureus (MRSA) are less common causes that predominantly occur in patients with specific risk factors. (See 'Microbiology' above and 'Pathogenesis' above.)

● Making the diagnosis – Diagnosis requires demonstration of an infiltrate on chest imaging in a patient with a clinically compatible syndrome (eg, fever, dyspnea, cough, and leukocytosis). For most patients, a posteroanterior and lateral chest radiograph is sufficient. Computed tomography scan is reserved for selected cases. (See 'Clinical presentation' above and 'Making the diagnosis' above.)

● Alternate and concurrent diagnoses – While the combination of a compatible clinical syndrome and an infiltrate on chest imaging are sufficient to establish an initial clinical diagnosis of CAP, these findings are nonspecific. Remaining attentive to the possibility of an alternate or concurrent diagnosis as a patient's course evolves is important to care. (See 'Differential diagnosis' above.)

● Determining severity of illness – For patients with a working diagnosis of CAP, the initial steps in management are defining the severity of illness and determining the most appropriate site of care ( algorithm 1 ). For most patients, we determine our approach to microbiologic testing based on this assessment ( table 5 ). (See 'Microbiologic testing' above.)

● Empiric antibiotic selection – The selection of an empiric antibiotic regimen is based on the severity of illness, site of care, and most likely pathogens. We generally start antibiotics as soon as we are confident that CAP is the appropriate working diagnosis and, ideally, within four hours of presentation for inpatients and within one hour of presentation for those who are critically ill (see 'Treatment' above):

• For most outpatients, we prefer to use combination therapy with a beta-lactam and either a macrolide (preferred) or doxycycline . Alternatives to beta-lactam-based regimens include monotherapy with either a fluoroquinolone or, alternatively, lefamulin or omadacycline (newer agents). Selection among these agents depends on patient comorbidities, drug interactions, allergies, and other intolerances. Clinical experience with lefamulin and omadacycline are limited; warnings and contraindications exist ( algorithm 2 ).

This approach differs from the American Thoracic Society/Infectious Diseases Society of America, which recommend monotherapy with amoxicillin as first line and monotherapy with either doxycycline or a macrolide (if local resistance rates are <25 percent [eg, not in the United States]) as alternatives for this population.

• For most inpatients admitted to the general medical ward, treatment options include either intravenous (IV) combination therapy with a beta-lactam plus a macrolide or doxycycline or monotherapy with a respiratory fluoroquinolone ( algorithm 3 ). These regimens should be expanded for patients with risk factors for Pseudomonas or MRSA ( table 4 ).

• For most patients admitted to the intensive care unit (ICU), treatment options include IV combination therapy with a beta-lactam plus either a macrolide or a respiratory fluoroquinolone ( algorithm 4 ). As with other hospitalized patients, regimens should be expanded for patients with risk factors for Pseudomonas or MRSA ( table 4 ).

● Adjunctive glucocorticoids – The benefit of adjunctive glucocorticoids appears greatest in patients with impending respiratory failure or requiring mechanical ventilation, particularly when they are given early in the course. Generally, we add hydrocortisone for most immunocompetent patients with respiratory failure due to CAP who require invasive or non-invasive mechanical ventilation or with significant hypoxemia (ie, PaO2:FIO2 ratio <300 with an FiO 2 requirement of ≥50 percent and use of either high flow nasal cannula or a nonrebreathing mask), unless there are reason to avoid their use (eg, infection with certain pathogen [influenza, fungi, tuberculosis, or immunocompromise]). (See 'Adjunctive glucocorticoids' above.)

● Directed antibiotic therapy – For patients in whom a causative pathogen has been identified, we tailor therapy to target the pathogen. (See 'Antibiotic de-escalation' above.)

● Duration of antibiotics – For all patients, we treat until the patient has been afebrile and clinically stable for at least 48 hours and for a minimum of five days. Patients with mild infection generally require five to seven days of therapy; those with severe infection or chronic comorbidities generally require 7 to 10 days of therapy. (See 'Duration of therapy' above.)

● Lack of response to antibiotics – Failure to respond to antibiotic treatment within 72 hours should prompt reconsideration of the diagnosis and empiric treatment regimen as well as an assessment for complications. (See 'Clinical failure' above and 'Nonresolving CAP' above.)

● Prevention – Key preventive measures include smoking cessation (when appropriate), influenza vaccination for the general population, and pneumococcal vaccination for at-risk populations. (See 'Prevention' above.)

ACKNOWLEDGMENT  —  UpToDate gratefully acknowledges John G Bartlett, MD (deceased), who contributed as Section Editor on earlier versions of this topic and was a founding Editor-in-Chief for UpToDate in Infectious Diseases.

• Mandell LA, Wunderink RG, Anzueto A, et al. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis 2007; 44 Suppl 2:S27.
• File TM. Community-acquired pneumonia. Lancet 2003; 362:1991.
• Musher DM, Thorner AR. Community-acquired pneumonia. N Engl J Med 2014; 371:1619.
• National Ambulatory Medical Care Survey (NAMCS) and National Hospital Ambulatory Medical Care Survey (NHAMCS) 2009 - 2010. https://www.cdc.gov/nchs/data/ahcd/combined_tables/2009-2010_combined_web_table01.pdf (Accessed on June 06, 2018).
• Xu J, Murphy SL, Kochanek KD, Bastian BA. Deaths: Final Data for 2013. Natl Vital Stat Rep 2016; 64:1.
• Pfuntner A, Wier LM, Stocks C. Most Frequent Conditions in U.S. Hospitals, 2011. HCUP Statistical Brief #162, Agency for Healthcare Research and Quality, Rockville, MD, September 2013.
• Ramirez JA, Wiemken TL, Peyrani P, et al. Adults Hospitalized With Pneumonia in the United States: Incidence, Epidemiology, and Mortality. Clin Infect Dis 2017; 65:1806.
• Jain S, Self WH, Wunderink RG, et al. Community-Acquired Pneumonia Requiring Hospitalization among U.S. Adults. N Engl J Med 2015; 373:415.
• Griffin MR, Zhu Y, Moore MR, et al. U.S. hospitalizations for pneumonia after a decade of pneumococcal vaccination. N Engl J Med 2013; 369:155.
• Almirall J, Bolíbar I, Balanzó X, González CA. Risk factors for community-acquired pneumonia in adults: a population-based case-control study. Eur Respir J 1999; 13:349.
• Torres A, Peetermans WE, Viegi G, Blasi F. Risk factors for community-acquired pneumonia in adults in Europe: a literature review. Thorax 2013; 68:1057.
• Bello S, Menéndez R, Antoni T, et al. Tobacco smoking increases the risk for death from pneumococcal pneumonia. Chest 2014; 146:1029.
• Wiese AD, Griffin MR, Schaffner W, et al. Opioid Analgesic Use and Risk for Invasive Pneumococcal Diseases: A Nested Case-Control Study. Ann Intern Med 2018; 168:396.
• Bain MR, Chalmers JW, Brewster DH. Routinely collected data in national and regional databases--an under-used resource. J Public Health Med 1997; 19:413.
• Curcio D, Cané A, Isturiz R. Redefining risk categories for pneumococcal disease in adults: critical analysis of the evidence. Int J Infect Dis 2015; 37:30.
• Johansson N, Kalin M, Tiveljung-Lindell A, et al. Etiology of community-acquired pneumonia: increased microbiological yield with new diagnostic methods. Clin Infect Dis 2010; 50:202.
• Musher DM, Roig IL, Cazares G, et al. Can an etiologic agent be identified in adults who are hospitalized for community-acquired pneumonia: results of a one-year study. J Infect 2013; 67:11.
• Musher DM, Abers MS, Bartlett JG. Evolving Understanding of the Causes of Pneumonia in Adults, With Special Attention to the Role of Pneumococcus. Clin Infect Dis 2017; 65:1736.
• Dickson RP, Erb-Downward JR, Martinez FJ, Huffnagle GB. The Microbiome and the Respiratory Tract. Annu Rev Physiol 2016; 78:481.
• Dickson RP, Erb-Downward JR, Huffnagle GB. Towards an ecology of the lung: new conceptual models of pulmonary microbiology and pneumonia pathogenesis. Lancet Respir Med 2014; 2:238.
• Faner R, Sibila O, Agustí A, et al. The microbiome in respiratory medicine: current challenges and future perspectives. Eur Respir J 2017; 49.
• Francis JS, Doherty MC, Lopatin U, et al. Severe community-onset pneumonia in healthy adults caused by methicillin-resistant Staphylococcus aureus carrying the Panton-Valentine leukocidin genes. Clin Infect Dis 2005; 40:100.
• Annane D, Renault A, Brun-Buisson C, et al. Hydrocortisone plus Fludrocortisone for Adults with Septic Shock. N Engl J Med 2018; 378:809.
• Moore M, Stuart B, Little P, et al. Predictors of pneumonia in lower respiratory tract infections: 3C prospective cough complication cohort study. Eur Respir J 2017; 50.
• Waterer GW, Kessler LA, Wunderink RG. Delayed administration of antibiotics and atypical presentation in community-acquired pneumonia. Chest 2006; 130:11.
• Metlay JP, Waterer GW, Long AC, et al. Diagnosis and Treatment of Adults with Community-acquired Pneumonia. An Official Clinical Practice Guideline of the American Thoracic Society and Infectious Diseases Society of America. Am J Respir Crit Care Med 2019; 200:e45.
• Fine MJ, Auble TE, Yealy DM, et al. A prediction rule to identify low-risk patients with community-acquired pneumonia. N Engl J Med 1997; 336:243.
• Lim WS, van der Eerden MM, Laing R, et al. Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study. Thorax 2003; 58:377.
• Marrie TJ, Lau CY, Wheeler SL, et al. A controlled trial of a critical pathway for treatment of community-acquired pneumonia. CAPITAL Study Investigators. Community-Acquired Pneumonia Intervention Trial Assessing Levofloxacin. JAMA 2000; 283:749.
• Yealy DM, Auble TE, Stone RA, et al. Effect of increasing the intensity of implementing pneumonia guidelines: a randomized, controlled trial. Ann Intern Med 2005; 143:881.
• Carratalà J, Fernández-Sabé N, Ortega L, et al. Outpatient care compared with hospitalization for community-acquired pneumonia: a randomized trial in low-risk patients. Ann Intern Med 2005; 142:165.
• Labarere J, Stone RA, Scott Obrosky D, et al. Factors associated with the hospitalization of low-risk patients with community-acquired pneumonia in a cluster-randomized trial. J Gen Intern Med 2006; 21:745.
• Liapikou A, Ferrer M, Polverino E, et al. Severe community-acquired pneumonia: validation of the Infectious Diseases Society of America/American Thoracic Society guidelines to predict an intensive care unit admission. Clin Infect Dis 2009; 48:377.
• Mandell LA. Severe community-acquired pneumonia (CAP) and the Infectious Diseases Society of America/American Thoracic Society CAP guidelines prediction rule: validated or not. Clin Infect Dis 2009; 48:386.
• Chalmers JD, Taylor JK, Mandal P, et al. Validation of the Infectious Diseases Society of America/American Thoratic Society minor criteria for intensive care unit admission in community-acquired pneumonia patients without major criteria or contraindications to intensive care unit care. Clin Infect Dis 2011; 53:503.
• Lim WS, Woodhead M, British Thoracic Society. British Thoracic Society adult community acquired pneumonia audit 2009/10. Thorax 2011; 66:548.
• Wunderink RG, Niederman MS, Kollef MH, et al. Linezolid in methicillin-resistant Staphylococcus aureus nosocomial pneumonia: a randomized, controlled study. Clin Infect Dis 2012; 54:621.
• Aliberti S, Zanaboni AM, Wiemken T, et al. Criteria for clinical stability in hospitalised patients with community-acquired pneumonia. Eur Respir J 2013; 42:742.
• Halm EA, Fine MJ, Marrie TJ, et al. Time to clinical stability in patients hospitalized with community-acquired pneumonia: implications for practice guidelines. JAMA 1998; 279:1452.
• Menéndez R, Torres A, Rodríguez de Castro F, et al. Reaching stability in community-acquired pneumonia: the effects of the severity of disease, treatment, and the characteristics of patients. Clin Infect Dis 2004; 39:1783.
• van der Eerden MM, Vlaspolder F, de Graaff CS, et al. Comparison between pathogen directed antibiotic treatment and empirical broad spectrum antibiotic treatment in patients with community acquired pneumonia: a prospective randomised study. Thorax 2005; 60:672.
• Ramirez JA, Srinath L, Ahkee S, et al. Early switch from intravenous to oral cephalosporins in the treatment of hospitalized patients with community-acquired pneumonia. Arch Intern Med 1995; 155:1273.
• Ramirez JA, Vargas S, Ritter GW, et al. Early switch from intravenous to oral antibiotics and early hospital discharge: a prospective observational study of 200 consecutive patients with community-acquired pneumonia. Arch Intern Med 1999; 159:2449.
• Di Pasquale MF, Sotgiu G, Gramegna A, et al. Prevalence and Etiology of Community-acquired Pneumonia in Immunocompromised Patients. Clin Infect Dis 2019; 68:1482.
• Ramirez JA, Musher DM, Evans SE, et al. Treatment of Community-Acquired Pneumonia in Immunocompromised Adults: A Consensus Statement Regarding Initial Strategies. Chest 2020; 158:1896.
• Menéndez R, Torres A, Zalacaín R, et al. Risk factors of treatment failure in community acquired pneumonia: implications for disease outcome. Thorax 2004; 59:960.
• Aliberti S, Amir A, Peyrani P, et al. Incidence, etiology, timing, and risk factors for clinical failure in hospitalized patients with community-acquired pneumonia. Chest 2008; 134:955.
• Rosón B, Carratalà J, Fernández-Sabé N, et al. Causes and factors associated with early failure in hospitalized patients with community-acquired pneumonia. Arch Intern Med 2004; 164:502.
• Arancibia F, Ewig S, Martinez JA, et al. Antimicrobial treatment failures in patients with community-acquired pneumonia: causes and prognostic implications. Am J Respir Crit Care Med 2000; 162:154.
• Violi F, Cangemi R, Falcone M, et al. Cardiovascular Complications and Short-term Mortality Risk in Community-Acquired Pneumonia. Clin Infect Dis 2017; 64:1486.
• Eurich DT, Marrie TJ, Minhas-Sandhu JK, Majumdar SR. Risk of heart failure after community acquired pneumonia: prospective controlled study with 10 years of follow-up. BMJ 2017; 356:j413.
• Ramirez J, Aliberti S, Mirsaeidi M, et al. Acute myocardial infarction in hospitalized patients with community-acquired pneumonia. Clin Infect Dis 2008; 47:182.
• Perry TW, Pugh MJ, Waterer GW, et al. Incidence of cardiovascular events after hospital admission for pneumonia. Am J Med 2011; 124:244.
• Warren-Gash C, Blackburn R, Whitaker H, et al. Laboratory-confirmed respiratory infections as triggers for acute myocardial infarction and stroke: a self-controlled case series analysis of national linked datasets from Scotland. Eur Respir J 2018; 51.
• Viasus D, Garcia-Vidal C, Manresa F, et al. Risk stratification and prognosis of acute cardiac events in hospitalized adults with community-acquired pneumonia. J Infect 2013; 66:27.
• Bruns AH, Oosterheert JJ, Cucciolillo MC, et al. Cause-specific long-term mortality rates in patients recovered from community-acquired pneumonia as compared with the general Dutch population. Clin Microbiol Infect 2011; 17:763.
• Dela Cruz CS, Wunderink RG, Christiani DC, et al. Future Research Directions in Pneumonia. NHLBI Working Group Report. Am J Respir Crit Care Med 2018; 198:256.
• Corrales-Medina VF, Alvarez KN, Weissfeld LA, et al. Association between hospitalization for pneumonia and subsequent risk of cardiovascular disease. JAMA 2015; 313:264.
• Fine MJ, Smith MA, Carson CA, et al. Prognosis and outcomes of patients with community-acquired pneumonia. A meta-analysis. JAMA 1996; 275:134.
• Lepper PM, Ott S, Nüesch E, et al. Serum glucose levels for predicting death in patients admitted to hospital for community acquired pneumonia: prospective cohort study. BMJ 2012; 344:e3397.
• Peyrani P, Ramirez JA. One-year mortality in patients with community-acquired pneumonia. Univ Louisville J Respir Infect 2017; 1.
• Eurich DT, Marrie TJ, Minhas-Sandhu JK, Majumdar SR. Ten-Year Mortality after Community-acquired Pneumonia. A Prospective Cohort. Am J Respir Crit Care Med 2015; 192:597.
• Mortensen EM, Kapoor WN, Chang CC, Fine MJ. Assessment of mortality after long-term follow-up of patients with community-acquired pneumonia. Clin Infect Dis 2003; 37:1617.
• Grohskopf LA, Sokolow LZ, Broder KR, et al. Prevention and Control of Seasonal Influenza With Vaccines: Recommendations of the Advisory Committee on Immunization Practices-United States, 2017-18 Influenza Season. Am J Transplant 2017; 17:2970.
• Tomczyk S, Bennett NM, Stoecker C, et al. Use of 13-valent pneumococcal conjugate vaccine and 23-valent pneumococcal polysaccharide vaccine among adults aged ≥65 years: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep 2014; 63:822.
• Centers for Disease Control and Prevention (CDC). Use of 13-valent pneumococcal conjugate vaccine and 23-valent pneumococcal polysaccharide vaccine for adults with immunocompromising conditions: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep 2012; 61:816.

• Patient Care & Health Information
• Diseases & Conditions

• Pneumonia and your lungs

Most pneumonia occurs when a breakdown in your body's natural defenses allows germs to invade and multiply within your lungs. To destroy the attacking organisms, white blood cells rapidly accumulate. Along with bacteria and fungi, they fill the air sacs within your lungs (alveoli). Breathing may be labored. A classic sign of bacterial pneumonia is a cough that produces thick, blood-tinged or yellowish-greenish sputum with pus.

Pneumonia is an infection that inflames the air sacs in one or both lungs. The air sacs may fill with fluid or pus (purulent material), causing cough with phlegm or pus, fever, chills, and difficulty breathing. A variety of organisms, including bacteria, viruses and fungi, can cause pneumonia.

Pneumonia can range in seriousness from mild to life-threatening. It is most serious for infants and young children, people older than age 65, and people with health problems or weakened immune systems.

Products & Services

• A Book: Living Medicine

The signs and symptoms of pneumonia vary from mild to severe, depending on factors such as the type of germ causing the infection, and your age and overall health. Mild signs and symptoms often are similar to those of a cold or flu, but they last longer.

Signs and symptoms of pneumonia may include:

• Chest pain when you breathe or cough
• Confusion or changes in mental awareness (in adults age 65 and older)
• Cough, which may produce phlegm
• Fever, sweating and shaking chills
• Lower than normal body temperature (in adults older than age 65 and people with weak immune systems)
• Nausea, vomiting or diarrhea
• Shortness of breath

Newborns and infants may not show any sign of the infection. Or they may vomit, have a fever and cough, appear restless or tired and without energy, or have difficulty breathing and eating.

When to see a doctor

See your doctor if you have difficulty breathing, chest pain, persistent fever of 102 F (39 C) or higher, or persistent cough, especially if you're coughing up pus.

It's especially important that people in these high-risk groups see a doctor:

• Adults older than age 65
• Children younger than age 2 with signs and symptoms
• People with an underlying health condition or weakened immune system
• People receiving chemotherapy or taking medication that suppresses the immune system

For some older adults and people with heart failure or chronic lung problems, pneumonia can quickly become a life-threatening condition.

There is a problem with information submitted for this request. Review/update the information highlighted below and resubmit the form.

From Mayo Clinic to your inbox

Sign up for free and stay up to date on research advancements, health tips, current health topics, and expertise on managing health. Click here for an email preview.

Error Email field is required

Error Include a valid email address

To provide you with the most relevant and helpful information, and understand which information is beneficial, we may combine your email and website usage information with other information we have about you. If you are a Mayo Clinic patient, this could include protected health information. If we combine this information with your protected health information, we will treat all of that information as protected health information and will only use or disclose that information as set forth in our notice of privacy practices. You may opt-out of email communications at any time by clicking on the unsubscribe link in the e-mail.

Thank you for subscribing!

You'll soon start receiving the latest Mayo Clinic health information you requested in your inbox.

Sorry something went wrong with your subscription

Please, try again in a couple of minutes

Many germs can cause pneumonia. The most common are bacteria and viruses in the air we breathe. Your body usually prevents these germs from infecting your lungs. But sometimes these germs can overpower your immune system, even if your health is generally good.

Pneumonia is classified according to the types of germs that cause it and where you got the infection.

Community-acquired pneumonia

Community-acquired pneumonia is the most common type of pneumonia. It occurs outside of hospitals or other health care facilities. It may be caused by:

• Bacteria. The most common cause of bacterial pneumonia in the U.S. is Streptococcus pneumoniae. This type of pneumonia can occur on its own or after you've had a cold or the flu. It may affect one part (lobe) of the lung, a condition called lobar pneumonia.
• Bacteria-like organisms. Mycoplasma pneumoniae also can cause pneumonia. It typically produces milder symptoms than do other types of pneumonia. Walking pneumonia is an informal name given to this type of pneumonia, which typically isn't severe enough to require bed rest.
• Fungi. This type of pneumonia is most common in people with chronic health problems or weakened immune systems, and in people who have inhaled large doses of the organisms. The fungi that cause it can be found in soil or bird droppings and vary depending upon geographic location.
• Viruses, including COVID-19 . Some of the viruses that cause colds and the flu can cause pneumonia. Viruses are the most common cause of pneumonia in children younger than 5 years. Viral pneumonia is usually mild. But in some cases it can become very serious. Coronavirus 2019 (COVID-19) may cause pneumonia, which can become severe.

Hospital-acquired pneumonia

Some people catch pneumonia during a hospital stay for another illness. Hospital-acquired pneumonia can be serious because the bacteria causing it may be more resistant to antibiotics and because the people who get it are already sick. People who are on breathing machines (ventilators), often used in intensive care units, are at higher risk of this type of pneumonia.

Health care-acquired pneumonia

Health care-acquired pneumonia is a bacterial infection that occurs in people who live in long-term care facilities or who receive care in outpatient clinics, including kidney dialysis centers. Like hospital-acquired pneumonia, health care-acquired pneumonia can be caused by bacteria that are more resistant to antibiotics.

Aspiration pneumonia

Aspiration pneumonia occurs when you inhale food, drink, vomit or saliva into your lungs. Aspiration is more likely if something disturbs your normal gag reflex, such as a brain injury or swallowing problem, or excessive use of alcohol or drugs.

Risk factors

Pneumonia can affect anyone. But the two age groups at highest risk are:

• Children who are 2 years old or younger
• People who are age 65 or older

Other risk factors include:

• Being hospitalized. You're at greater risk of pneumonia if you're in a hospital intensive care unit, especially if you're on a machine that helps you breathe (a ventilator).
• Chronic disease. You're more likely to get pneumonia if you have asthma, chronic obstructive pulmonary disease ( COPD ) or heart disease.
• Smoking. Smoking damages your body's natural defenses against the bacteria and viruses that cause pneumonia.
• Weakened or suppressed immune system. People who have HIV / AIDS , who've had an organ transplant, or who receive chemotherapy or long-term steroids are at risk.

Complications

Even with treatment, some people with pneumonia, especially those in high-risk groups, may experience complications, including:

• Bacteria in the bloodstream (bacteremia). Bacteria that enter the bloodstream from your lungs can spread the infection to other organs, potentially causing organ failure.
• Difficulty breathing. If your pneumonia is severe or you have chronic underlying lung diseases, you may have trouble breathing in enough oxygen. You may need to be hospitalized and use a breathing machine (ventilator) while your lung heals.
• Fluid accumulation around the lungs (pleural effusion). Pneumonia may cause fluid to build up in the thin space between layers of tissue that line the lungs and chest cavity (pleura). If the fluid becomes infected, you may need to have it drained through a chest tube or removed with surgery.
• Lung abscess. An abscess occurs if pus forms in a cavity in the lung. An abscess is usually treated with antibiotics. Sometimes, surgery or drainage with a long needle or tube placed into the abscess is needed to remove the pus.

To help prevent pneumonia:

• Get vaccinated. Vaccines are available to prevent some types of pneumonia and the flu. Talk with your doctor about getting these shots. The vaccination guidelines have changed over time so make sure to review your vaccination status with your doctor even if you recall previously receiving a pneumonia vaccine.
• Make sure children get vaccinated. Doctors recommend a different pneumonia vaccine for children younger than age 2 and for children ages 2 to 5 years who are at particular risk of pneumococcal disease. Children who attend a group child care center should also get the vaccine. Doctors also recommend flu shots for children older than 6 months.
• Practice good hygiene. To protect yourself against respiratory infections that sometimes lead to pneumonia, wash your hands regularly or use an alcohol-based hand sanitizer.
• Don't smoke. Smoking damages your lungs' natural defenses against respiratory infections.
• Keep your immune system strong. Get enough sleep, exercise regularly and eat a healthy diet.
• Pneumonia. National Heart, Lung, and Blood Institute. http://www.nhlbi.nih.gov/health/health-topics/topics/pnu. Accessed April 15, 2016.
• AskMayoExpert. Community-acquired pneumonia (adult). Rochester, Minn.: Mayo Foundation for Medical Education and Research; 2014.
• Goldman L, et al., eds. Overview of pneumonia. In: Goldman-Cecil Medicine. 25th ed. Philadelphia, Pa.: Saunders Elsevier; 2016. http://www.clinicalkey.com. Accessed April 18, 2016.
• Schauner S, et al. Community-acquired pneumonia in children: A look at the IDSA guidelines. Journal of Family Practice. 2013;62:9.
• Attridge RT, et al. Health care-associated pneumonia: An evidence-based review. American Journal of Medicine. 2011;124:689.
• Hunter JD. Ventilator associated pneumonia. BMJ. 2012;344:e3325.
• Dockrell DH, et al. Pneumococcal pneumonia: Mechanisms of infection and resolution. Chest. 2012;142:482.
• Reynolds RH, et al. Pneumonia in the immunocompetent patient. British Journal of Radiology. 2010;83:998.
• Remington LT, et al. Community-acquired pneumonia. Current Opinion Pulmonary Medicine. 2014;20:215.
• Centers for Disease Control and Prevention. Adults: Protect yourself with pneumococcal vaccines. http://www.cdc.gov/features/adult-pneumococcal/. Accessed April 15, 2016.
• Marrie TJ, et al. Pneumococcal pneumonia in adults. http://www.uptodate.com/home. Accessed April 15, 2016.
• Barbara Woodward Lips Patient Education Center. Care following hospitalization for community-acquired pneumonia. Rochester, Minn.: Mayo Foundation for Medical Education and Research; 2013.
• AskMayoExpert. Community-acquired pneumonia (pediatric). Rochester, Minn.: Mayo Foundation for Medical Education and Research; 2014.
• Barson WJ. Community-acquired pneumonia in children: Outpatient treatment. http://www.uptodate.com/home. Accessed April 15, 2016.
• File TM. Treatment of community-acquired pneumonia in adults in the outpatient setting. http://www.uptodate.com/home. Accessed April 20, 2016.
• Chang CC, et al. Over-the-counter ( OTC ) medications to reduce cough as an adjunct to antibiotics for acute pneumonia in children and adults. Cochrane Database of Systematic Reviews. http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD006088.pub4/full. Accessed April 20, 2016.
• Mycoplasma pneumoniae infection. Centers for Disease Control and Prevention. http://www.cdc.gov/pneumonia/atypical/mycoplasma/. Accessed April 20, 2016.
• Barson WJ. Community-acquired pneumonia in children: Clinical features and diagnosis. http://www.uptodate.com/home. Accessed April 20, 2016.
• Olson EJ (expert opinion). Mayo Clinic, Rochester, Minn. May 1, 2016.
• AskMayoExpert. COVID-19: Outpatient. Mayo Clinic; 2020.
• Chest X-ray showing pneumonia
• Walking pneumonia

Associated Procedures

• Chest X-rays
• Extracorporeal membrane oxygenation (ECMO)
• Symptoms & causes
• Diagnosis & treatment
• Doctors & departments

Mayo Clinic does not endorse companies or products. Advertising revenue supports our not-for-profit mission.

• Opportunities

Mayo Clinic Press

Check out these best-sellers and special offers on books and newsletters from Mayo Clinic Press .

• Mayo Clinic on Incontinence - Mayo Clinic Press Mayo Clinic on Incontinence
• The Essential Diabetes Book - Mayo Clinic Press The Essential Diabetes Book
• Mayo Clinic on Hearing and Balance - Mayo Clinic Press Mayo Clinic on Hearing and Balance
• FREE Mayo Clinic Diet Assessment - Mayo Clinic Press FREE Mayo Clinic Diet Assessment
• Mayo Clinic Health Letter - FREE book - Mayo Clinic Press Mayo Clinic Health Letter - FREE book

Make twice the impact

Your gift can go twice as far to advance cancer research and care!

Home Collections Medical Clinical Pneumonia Case

Best Clinical Pneumonia Case PowerPoint And Google Slides

Clinical Pneumonia Case Presentation Slides

Features of the template:.

• 100% customizable slide and easy to download.
• The slide contains 16:9 and 4:3 format.
• Well-crafted template with an instant download facility.
• Highly compatible with PowerPoint and Google Slides.
• This slide has a colorful design pattern.
• Easy to change the slide colors.
• Clinical Case Of Pneumonia
• Lung Disease
• Pediatric Pneumonia
• Pneumonia Clinical Case
• Google Slides

669+ Templates

124+ Templates

Science & Research

182+ Templates

Telemedicine

40+ Templates

323+ Templates

86+ Templates

116+ Templates

44+ Templates

191+ Templates

You May Also Like These PowerPoint Templates

Got any suggestions?

We want to hear from you! Send us a message and help improve Slidesgo

Top searches

Trending searches

memorial day

12 templates

17 templates

26 templates

20 templates

american history

73 templates

11 templates

Clinical Case of Pneumonia

Clinical case of pneumonia presentation, free google slides theme, powerpoint template, and canva presentation template.

This clinical case template is formal and perfect for medical topics. The backgrounds are blue and they show gradients and geometric shapes, which look very professional. This theme contains pictures of physicians and diagrams of lungs. The sans serif titles reminisce about posters, which complements the style of the slides.

Features of this template

• A formal design with geometric gradients
• 100% editable and easy to modify
• 29 different slides to impress your audience
• Contains easy-to-edit graphics, maps and mockups
• Includes 500+ icons and Flaticon’s extension for customizing your slides
• Designed to be used in Google Slides, Canva, and Microsoft PowerPoint
• 16:9 widescreen format suitable for all types of screens
• Includes information about fonts, colors, and credits of the free resources used

How can I use the template?

Am I free to use the templates?

How to attribute?

Attribution required If you are a free user, you must attribute Slidesgo by keeping the slide where the credits appear. How to attribute?

Related posts on our blog.

How to Add, Duplicate, Move, Delete or Hide Slides in Google Slides

How to Change Layouts in PowerPoint

How to Change the Slide Size in Google Slides

Related presentations.

Premium template

Unlock this template and gain unlimited access

• Case report
• Open access
• Published: 30 April 2024

Refractory pneumonia caused by Prevotella heparinolytica : a case report

• Jiongzhou Sun 1 ,
• Shiyuan Gao 1 ,
• Qiong Pan 1 ,
• Zian Liu 1 ,
• Yiwen Huang 1 &
• Yixin Lian 1  

Journal of Medical Case Reports volume  18 , Article number:  213 ( 2024 ) Cite this article

90 Accesses

1 Altmetric

Metrics details

Prevotella heparinolytica is a Gram-negative bacterium that is commonly found in the oral, intestinal, and urinary tracts. It has been extensively studied in lower respiratory tract infections in horses, which has heparinolytic activity and can secrete heparinase and further induces virulence factors in cells and causes disease. However, no such cases have been reported in humans.

Case presentation

A 58-year-old male patient from China presented to the respiratory clinic in Suzhou with a productive cough producing white sputum for 20 days and fever for 3 days. Prior to this visit, a chest computed tomography scan was conducted, which revealed multiple patchy nodular opacities in both lungs. On admission, the patient presented with a temperature of 38.1 °C and a pulse rate of 110 beats per minute. Despite routine anti-infective treatment with moxifloxacin, his temperature fluctuated and the treatment was ineffective. The patient was diagnosed with Prevotella heparinolytica infection through metagenomic next-generation sequencing. Therefore, the antibiotics were switched to piperacillin–tazobactam in combination with ornidazole, which alleviated his symptoms; 1 week after discharge, the patient returned to the clinic for a follow-up chest computed tomography, and the opacities on the lungs continued to be absorbed.

Prevotella heparinolytica is an opportunistic pathogen. However, it has not been reported in human pneumonia. In refractory pneumonia, measures such as metagenomic next-generation sequencing can be used to identify pathogens and help guide antibiotic selection and early support.

Peer Review reports

Prevotella heparinolytica, also known as Bacteroides heparinolyticus , is a Gram-negative bacterium that is exclusively anaerobic. It is commonly found in the oral, intestinal, and urinary tracts. Prevotella heparinolytica produces heparinase and hyaluronidase, which increase epithelial permeability by degrading acetylheparin sulfate in the intercellular space and bound to the epithelial basement membrane [ 1 , 2 ]. The release of microbial virulence factors can contribute to the development of diseases, such as periodontal disease. Therefore, it is important to consider this factor in disease prevention and treatment.

Studies have reported that Prevotella heparinolytica is the dominant bacterium in equine lower respiratory tract infections [ 3 ]. It is believed that there is an association between this condition and oral diseases, such as periodontitis, in humans [ 4 , 5 ]. However, there are no case reports of lower respiratory tract infections associated with Prevotella heparinolytica in humans. This report presents a case of pneumonia in a patient who sought medical attention due to cough and fever caused by Prevotella heparinolytica .

A 58-year-old Chinese male patient presented to the respiratory clinic in Suzhou, China, with a productive cough with white sputum for 20 days and fever for 3 days. A computed tomography (CT) scan of the chest was conducted 2 weeks prior, which showed several patchy nodular opacities in both lungs. He was prescribed oral medications, including methylprednisolone 4 mg once a day and celecoxib 0.2 g once a day for 3 days. This led to some relief of his cough. Prior to admission, the patient experienced a 3-day episode of coughing with white sputum and a fever (axillary temperature of 38 °C). The patient had a history of hypertension and was taking amlodipine 5 mg once a day. He worked as a farmer and reported no history of smoking, alcohol consumption, or contact with poultry. There was no family history of genetic or psychosocial disorders or surgeries. The patient did not report any travel to epidemic areas or contact with febrile patients.

On admission on 19 February, the patient walked into the ward and was conscious. His vital signs were as follows: axillary temperature was 38.1 °C, pulse rate was 110 beats per minute, respiratory rate was 22 breaths per minute, blood pressure was 135/76 mmHg, and pulse oximetry on air was 96%. Few moist rales were heard upon auscultation of his lungs. Abdominal, neurological, and skin examinations were normal, and no heart murmur was detected during cardiac auscultation.

On the day of the presentation, a repeat chest CT revealed multiple opacities in both lungs and progression compared with previous images (Fig.  1 a, b). Simultaneously, several laboratory investigations were conducted on blood and sputum samples. The patient’s white blood cell count was 21.5 × 10 9 /L (reference 3.5–9.5 × 10 9 /L), of which 88.6% were neutrophils (in absolute number 19.0 × 10 9 /L). Procalcitonin (PCT) levels were elevated, as well as d -dimer levels. The patient’s C-reactive protein (CRP) level was significantly increased at 186.9 mg/L (reference 0–10 mg/L). Bilateral blood cultures for anaerobes and aerobes were taken upon admission and yielded negative results. The results of other aetiological detection, such as the acid-fast bacillus test of sputum smear, coronavirus nucleic acid, 1,3-beta- d -glucan, galactomannan test, and antibodies for common respiratory pathogens, including Mycoplasma pneumoniae , Chlamydia pneumoniae , respiratory syncytial virus, adenovirus and coxsackievirus group B, were all negative (Table  1 ). The patient’s urinalysis, liver function, and renal function tests all returned normal results. Additionally, the sputum culture was negative. According to the patient’s laboratory results, which included tumour indicators, antineutrophil cytoplasmic antibodies (ANCA), and human immunodeficiency virus antibodies, there was no indication of tumours or immune system disorders at that time.

Chest computed tomography performed at different times. a, b Computed tomography image of the patient after admission to the hospital on hospitalization day 1 due to fever. c, d Computed tomography image 12 days after discharge

The patient was given intravenous moxifloxacin 0.4 g once a day as an empirical anti-infective treatment in the hospital. However, he still had a low fever with paroxysmal cough. As moxifloxacin did not alleviate the symptoms and C-reactive protein (CRP) levels remained high, a bronchoscopy was performed on 21 February. During the procedure, a brush examination was conducted on the apical and posterior segments of the right upper lobe of the lung. The samples underwent routine pathogenetic testing and metagenomic next-generation sequencing (mNGS). Results showed Prevotella heparinolytica was detected (sequence number 1620, relative abundance 55.69%) in mNGS (Table  2 ). The samples obtained through sterile bronchoscopy underwent a bacterial smear test, which detected Gram-negative bacilli. This result was consistent with the mNGS findings. Additionally, bronchoscopy did not reveal any evidence of neoplasm. Moreover, bacterial and fungal culture tests were conducted, all of which yielded negative results. Therefore, susceptibility testing was not performed. On the basis of the patient’s medical history, it was found that he had developed periodontitis 1 month prior. However, self-treatment with metronidazole was found to be ineffective. During the examination, it was observed that the patient had a loose left maxillary second molar. The gingiva appeared red and swollen. The patient reported pain while chewing, and the tooth was sensitive to hot and cold food. Following a dental consultation, the patient was diagnosed with periodontitis. It was noted that Prevotella heparinolytica can colonize the oral cavity. Considering the patient’s history of recurrent episodes and ineffective antibiotic therapy, it cannot be ruled out that there is a correlation between oral and pulmonary infections. On the basis of the history and examination results, it was considered that the patient has a pulmonary infection caused by Prevotella heparinolytica .

Due to its higher in vivo anti-anaerobic activity, faster onset of action, and lower toxicity, the patient’s antibiotics were changed to 0.5 g of ornidazole every 12 hours combined with piperacillin-tazobactam (4.5 g per 6 hours intravenously) on 23 February for 5 days. The patient’s fever and cough symptoms gradually subsided, and his inflammatory markers, including white blood cell count (WBC, 7.3 × 10 9 /L) and CRP (15.5 mg/L), improved compared with admission. On 28 February, a chest CT revealed a marked improvement in lung inflammation. The patient was discharged on 1 March and continued oral amoxicillin 0.5 g three times daily and moxifloxacin 0.4 g once daily for 2 weeks. On 13 March, 12 days after discharge, the patient returned to the hospital for a follow-up CT (Fig.  1 c, d). The inflammation in the postapical segment of the upper lobe of the right lung and the lingual segment of the upper lobe of the left lung continued to subside. Figure  2 presents the patient’s symptoms, examinations, and treatments.

Timeline of the clinical events of the patient

This report describes a case of refractory pneumonia caused by Prevotella heparinolytica in a middle-aged male patient with a long-standing illness. The main symptoms were cough and fever, and imaging revealed multiple plaque-like nodules in both lungs. It is important to note that respiratory physicians may be less familiar with Prevotella heparinolytica .

Prevotella heparinolytica , once known as Bacteroides heparinolyticus , was first described in the human oral cavity by Nakamura. It is a Gram-negative anaerobe that is commonly found in the oral cavity and other tracts. It has heparinolytic activity [ 1 , 4 ] and secretes a heparinase enzyme that is believed to bind and degrade acetylated heparan sulfate in the intercellular space and epithelial basement membrane. This process allows virulence factors produced by the microorganism to enter the epithelium [ 6 ].

There have been studies of horse infections with Prevotella heparinolytica , but no such cases have been reported in humans. In horse lower respiratory tract infections, specific anaerobes are important pathogens for pneumonia or pleuropneumonia, and Prevotella heparinolytica is the common dominant organism in horse pulmonary infections. A study by Yuta Kinoshita et al . proposed that most Prevotella isolates are susceptible to β-lactams and that all Bacteroides and Prevotella isolates are susceptible to metronidazole [ 3 ]. Laura et al . demonstrated that Prevotella  spp. can produce β-lactamase and are sensitive to meropenem, piperacillin-tazobactam, chloramphenicol, and metronidazole [ 7 ]. As for Prevotella heparinolytica , it is often sensitive to metronidazole, imipenem and clindamycin. The patient’s anti-infection measures were changed to piperacillin-tazobactam combined with venous ornidazole due to its higher in vivo anti-anaerobic activity, faster onset of action, and lower toxicity.

On admission, the patient was diagnosed with community-acquired pneumonia, sepsis, and hypertension. The patient’s oral health was found to be poor despite the absence of an immune system disorder. The mNGS identified the pathogen responsible for the infection, with Prevotella heparinolytica detected. Treatment consisted of a combination of penicillin and anti-nitroimidazoles, resulting in significant improvement of the patient’s symptoms and imaging manifestations, we considered him to be infected by Prevotella heparinolytica .

For patients with refractory or severe pneumonia, early identification of pathogens is crucial for adjusting anti-infective drugs. However, the use of traditional methods, such as bacterial culture and immunological tests, is somewhat limited due to poor timeliness and low positivity rates [ 8 ]. The identification of Prevotella heparinolytica can be challenging using culture-based methods, but molecular diagnostic techniques can provide valuable insights into the detection of this pathogen [ 2 ]. Can Chang et al . analysed a clinical sample of 180 patients and found that the positive rate of microorganisms detected by mNGS was significantly higher compared with conventional microbiological tests [ 9 ]. Bronchoalveolar lavage fluid (BALF) is currently the recommended source of samples for testing. This helps to minimize the effects of oral colonization of bacteria and provides a representative sample of the alveolar components [ 10 ]. However, it should be noted that there are still some limitations to consider. The results may be influenced by specimen contamination, bacterial colonization, and the immunocompromised status of the patient. Therefore, in clinical applications, mNGS is significant for diagnosing diseases and guiding treatment. However, the interpretation of its results should take into account microorganisms, host factors, and the patient’s clinical manifestations.

Moreover, in the case of pulmonary infections, clinicians need to be concerned about specific pathogens, such as oral infections and oral-colonizing bacteria. It is well documented that diseases such as periodontitis and dental caries have an impact on lower respiratory tract diseases. Aspiration pneumonia is a frequent lung infection caused by oropharyngeal colonizing bacteria that enter the lower respiratory tract through inhalation, leading to disease. This is often observed in patients who are at a higher risk of aspirating oral contents, such as those with impaired consciousness [ 11 , 12 ]. Patients who suffer from oral infections exhibit increased levels of hydrolases in their saliva. These enzymes can compromise the protective barrier that prevents bacterial penetration [ 13 ]. Bacteria associated with periodontal disease, such as Prevotella spp. and Clostridium spp., are thought to be involved in the progression of aspiration pneumonia [ 14 ]. Research indicates that periodontal diseases, including chronic periodontal inflammation, are prevalent in 20–50% of the global population [ 15 ]. Furthermore, chronic inflammation can spread systemically through the vascular system, potentially impacting conditions such as community-acquired pneumonia, chronic obstructive pulmonary disease, atherosclerosis, and diabetes [ 16 ]. According to some theories, systemic disease may be caused by microorganisms in local oral cavity infections due to the widespread presence of bacteria and their metabolites [ 17 ]. Numerous studies have been conducted on the correlation between the oral environment and lung infections. Patients with moderate-to-severe chronic periodontitis are at a significantly higher risk of developing community-acquired pneumonia than the general population [ 18 ]. In a follow-up study of elderly patients, researchers found an increased mortality rate from pneumonia in patients with an increased number and size of periodontal pockets compared with those without pockets [ 19 ]. Oral health has an impact on the incidence and progression of lung infections. Patients with lung infections are sometimes treated empirically due to a lack of characteristic symptoms and imaging. However, those with persistent symptoms need to be actively identified for pathogens, and early pathogenic investigations are necessary. Several studies have shown that oral bacteria can have an impact on the onset and course of lung infections [ 20 ]. Therefore, oral care plays a vital role in preventing lung infections, not only in elderly individuals, but also in the clinical management process.

Prevotella heparinolytica is a low-virulence pathogen that can colonise natural cavities, such as the oral cavity, and cause lung infections. Infections typically follow a subacute course. Early diagnosis and effective anti-infection measures can lead to patient recovery. mNGS has shown high sensitivity and specificity in identifying pathogens, making it a promising diagnostic method to complement conventional microbiological tests.

Availability of data and materials

All data pertaining to this patient are included in this report.

Abbreviations

Computed tomography

• Metagenomics next-generation sequencing

Bronchoalveolar lavage fluid

Watanabe M, Tsuda H, Yamada S, et al . Characterization of heparinase from an oral bacterium Prevotella heparinolytica . J Biochem. 1998;123(2):283–8.

Article   CAS   PubMed   Google Scholar  

Ashimoto A, Flynn MJ, Slots J. Molecular genetic detection of Bacteroides heparinolyticus in adult periodontitis. Oral Microbiol Immunol. 1995;10(5):284–7.

Kinoshita Y, Niwa H, Katayama Y, Hariu K. Dominant obligate anaerobes revealed in lower respiratory tract infection in horses by 16S rRNA gene sequencing. J Vet Med Sci. 2014;76(4):587–91.

Article   PubMed   Google Scholar  

Bailey GD, Moore LVH, Love DN, Johnson JL. Bacteriodes heparinolyticus: deoxyribonucleic acid relatedness of strains from the oral cavity and oral-associated disease conditions of horses, cats, and humans. Int J Syst Bacteriol. 1988;38(1):42–4.

Article   CAS   Google Scholar  

Love DN, Johnson JL, Moore LV. Bacteroides species from the oral cavity and oral-associated diseases of cats. Vet Microbiol. 1989;19(3):275–81.

Smith AJ, Greenman J, Embery G. Detection and possible biological role of chondroitinase and heparitinase enzymes produced by Porphyromonas gingivali s W50. J Periodontal Res. 1997;32(1):1–8.

Sherrard LJ, Graham KA, McGrath SJ, et al . Antibiotic resistance in Prevotella species isolated from patients with cystic fibrosis. J Antimicrob Chemother. 2013;68(10):2369–74.

Article   CAS   PubMed   PubMed Central   Google Scholar  

Gu W, Deng X, Lee M, et al . Rapid pathogen detection by metagenomic next-generation sequencing of infected body fluids. Nat Med. 2021;27(1):115–24.

Chang C, Wang H, Zhang L, et al . Clinical efficiency of metagenomic next-generation sequencing in sputum for pathogen detection of patients with pneumonia according to disease severity and host immune status. Infect Drug Resist. 2023;16:5869–85.

Yang A, Chen C, Hu Y, et al . Application of metagenomic next-generation sequencing (mNGS) using bronchoalveolar lavage fluid (BALF) in diagnosing pneumonia of children. Microbiol Spectr. 2022;10(5):e01488.

Article   PubMed   PubMed Central   Google Scholar  

Racklyeft DJ, Love DN. Bacterial infection of the lower respiratory tract in 34 horses. Aust Vet J. 2000;78(8):549–59.

Scannapieco FA, Cantos A. Oral inflammation and infection, and chronic medical diseases: implications for the elderly. Periodontol 2000. 2016;72(1):153–75.

Debelian GJ, Olsen I. Systemic diseases caused by oral infection. Clin Microbiol Rev. 2000;13(4):547–8.

Article   Google Scholar  

Seymour GJ, Ford PJ, Cullinan MP, et al . Relationship between periodontal infections and systemic disease. Clin Microbiol Infect. 2007;13(Suppl 4):3–10.

Maurin M. Editorial: Insights in clinical microbiology: 2021. Front Cell Infect Microbiol. 2022;12: 928344.

Molina A, Huck O, Herrera D, Montero E. The association between respiratory diseases and periodontitis: a systematic review and meta-analysis. J Clin Periodontol. 2023;50(6):842–87.

Mammen MJ, Scannapieco FA, Sethi S. Oral–lung microbiome interactions in lung diseases. Periodontol 2000. 2020;83(1):234–41.

De Melo Neto JP, Melo MSAE, Dos Santos-Pereira SA, et al . Periodontal infections and community-acquired pneumonia: a case–control study. Eur J Clin Microbiol Infect Dis. 2013;32(1):27–32.

Awano S, Ansai T, Takata Y, et al . Oral health and mortality risk from pneumonia in the elderly. J Dent Res. 2008;87(4):334–9.

Imai K, Iinuma T, Sato S. Relationship between the oral cavity and respiratory diseases: aspiration of oral bacteria possibly contributes to the progression of lower airway inflammation. Jpn Dent Sci Rev. 2021;57:224–30.

Download references

Acknowledgements

This study was supported by the Suzhou Science and Technology Development Program (SYSD2019104), the Medical Science Research Funding Project of Beijing Medical Health Public Welfare Foundation (YWJKJJHKYJJ-HX05), and the Advanced Research Funding Program of The Second Affiliated Hospital of Soochow University (SDFEYBS2002 and SDFEYHT2224).

Author information

Authors and affiliations.

Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China

Jiongzhou Sun, Xun Xu, Shiyuan Gao, Qiong Pan, Zian Liu, Yiwen Huang & Yixin Lian

You can also search for this author in PubMed   Google Scholar

Contributions

The first draft of the manuscript was written by JS. XX and YL reviewed the manuscript for intellectual content. SG and XX were involved in the management of the patient. QP, ZL, and YH collected the data. All authors critically revised the manuscript and approved the final version.

Corresponding authors

Correspondence to Xun Xu or Yixin Lian .

Ethics declarations

Ethics approval and consent to participate.

Approval from an ethics committee was not needed for this case report since it involved one patient.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare that they have no competing interests.

Additional information

Publisher’s note.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ . The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/ ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Cite this article.

Sun, J., Xu, X., Gao, S. et al. Refractory pneumonia caused by Prevotella heparinolytica : a case report. J Med Case Reports 18 , 213 (2024). https://doi.org/10.1186/s13256-024-04538-8

Download citation

Received : 26 October 2023

Accepted : 03 April 2024

Published : 30 April 2024

DOI : https://doi.org/10.1186/s13256-024-04538-8

Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

• Prevotella heparinolytica
• Oral infections

Journal of Medical Case Reports

ISSN: 1752-1947

• Submission enquiries: Access here and click Contact Us
• General enquiries: [email protected]