Last reviewed: 25 Aug 2022
Last updated: 22 Dec 2021

Introduction

Condition
Description

Community-acquired pneumonia (CAP) is defined as pneumonia acquired outside hospital or healthcare facilities. Patients with CAP typically present with signs and symptoms of lower respiratory tract infection (i.e., cough, dyspnea, pleuritic chest pain, mucopurulent sputum, myalgia, fever).[1]Older people present more frequently with confusion or worsening of pre-existing conditions, without chest signs or fever.[2] Bacterial and viral pathogens are the leading cause of CAP; most infections are caused by Streptococcus pneumoniae (also known as pneumococcus). Clinical judgement along with a validated prediction rule for prognosis are used to determine the need for hospital admission in adults with CAP.[3] Radiographic confirmation of the diagnosis (presence of new consolidation on a chest radiograph) should be obtained in hospitalized patients.

Hospital-acquired pneumonia (HAP) is an acute lower respiratory tract infection that is by definition acquired after at least 48 hours of admission to the hospital and is not incubating at the time of admission.[4] The spectrum of HAP is now distinct from ventilator-associated pneumonia (VAP), which is defined as pneumonia occurring more than 48 hours after endotracheal intubation. Healthcare-associated pneumonia (HCAP) is no longer considered a clinical entity in the 2016 guidelines for HAP and VAP by the Infectious Diseases Society and the American Thoracic Society.[4] HAP and VAP are usually due to bacterial infection, and the timely initiation of appropriate antimicrobial therapy is a key prognostic factor.[5] 

Viral pneumonia (non COVID-19)

Viral pathogens are frequently responsible for both community-acquired and hospital-acquired pneumonias. Infection is often caused by influenza virus, respiratory syncytial virus (RSV), or parainfluenza virus; of these, influenza virus is the leading cause in adults.[6] Patients at the extremes of age, and individuals with immune suppression of any cause, including pregnancy, are at increased risk of viral pneumonia. The clinical features are nonspecific, but a diagnosis can be made by isolating viral nucleic acid from respiratory tract secretions.[7] Coinfection with a viral and bacterial pathogen, or superadded bacterial infection, is associated with increased bacterial virulence, and greater morbidity and mortality. Commonly implicated microorganisms include influenza virus, RSV, parainfluenza virus, and human metapneumovirus; complicated by infection with Staphylococcus aureus, Streptococcus pneumoniae, and Haemophilus influenzae.[8]

An acute respiratory infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It was first identified in Wuhan City, Hubei Province, China, in December 2019. Since then it has spread to many countries around the world, with the World Health Organization declaring it a pandemic.

An acute viral respiratory tract infection caused by SARS-CoV.[9] It was first identified in the Guangdong province of Southern China in 2002. The epidemic affected 26 countries and resulted in more than 8000 cases and 774 deaths in 2003. There have been no reported cases since 2004. The case fatality rate is approximately 10%. [10]

An acute viral respiratory tract infection caused by MERS-CoV. It was first identified in Saudi Arabia in 2012. Cases have been limited to the Arabian Peninsula and its surrounding countries, and to travelers from the Middle East or their contacts. The case fatality rate is approximately 37%.[11]

Atypical bacterial pneumonia is caused by atypical organisms that are not detectable on Gram stain and cannot be cultured using standard methods. The most common organisms are Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Legionella pneumophila.[12] Atypical bacterial pneumonia is usually characterized by a symptom complex that includes headache, low-grade fever, cough, and malaise. Constitutional symptoms often predominate over respiratory findings, and there may be extrapulmonary manifestations. In most cases, presentation is in the milder spectrum of community-acquired pneumonia; however, infection may result in a severe pneumonia, necessitating intensive care admission. Patients who are hospitalized with atypical infection tend to be younger, and are less likely to have cardiovascular, renal, or metabolic comorbidities, than those with non-atypical pneumonia.[13]

Mycoplasma pneumoniae causes community-acquired pneumonia and upper respiratory illness. Patients may present with symptoms including an unresolved persistent cough, low-grade fever, headache, hoarseness, rash, and, rarely, bullous myringitis.M pneumoniae occurs mainly in children and young adults, and is often seen in close community settings (e.g., boarding schools, army bases, and universities).[12] The diagnosis is usually made clinically, but can be confirmed using nucleic acid amplification tests or cultures.

Chlamydia pneumoniae is a common cause of acute respiratory tract infection in all age groups, worldwide. Infection with C pneumoniae accounts for around 10% of cases of community-acquired pneumonia.[14] The clinical features are nonspecific and wide-ranging, but classically include a fever and cough, preceded by upper respiratory tract symptoms.[15] Pneumonia due to C pneumoniae cannot be differentiated clinically from other atypical pneumonia-causing organisms, especially Mycoplasma pneumoniae.[16] The diagnosis can be confirmed using nucleic acid amplification tests.

Legionella pneumonia, known as Legionnaires' disease, occurs when the bacteria are inhaled (or rarely aspirated) into the lungs. Almost all cases of community-acquired Legionnaires' disease are associated with contaminated aerosols produced by man-made water systems.[17] Presentation includes respiratory symptoms such as cough (may not be productive) and shortness of breath, fever, chills, and chest pain. Other symptoms include headache, nausea, vomiting, abdominal pain, or diarrhea. Legionella pneumophila infection may result in a severe pneumonia, necessitating intensive care unit admission.[18]

Pneumocystis pneumonia (PCP) is an infection of the lungs caused by the fungal organism Pneumocystis jirovecii (formerly known as Pneumocystis carinii). Typically, it causes clinical disease in severely immunocompromised patients, such as HIV-infected people with CD4+ count <200 cells/microliter, hematopoietic cell transplant patients, solid-organ transplant patients, or patients on chronic immunosuppressive therapy. 

Coccidioidomycosis is a fungal infection caused by endemic Coccidioides species found within areas of the southwest US, northern Mexico, and limited areas of Central and South America. Infection is acquired through the inhalation of airborne arthrospores; it may be asymptomatic or can cause acute and chronic pulmonary syndrome, and, rarely, extrapulmonary infection. [19]

Aspergillosis is an infection caused by inhalation of the aerosolized conidia (spores) of the Aspergillus fungus, which is found ubiquitously in soil. Aspergillosis mostly affects immunocompromised patients and is rare in immunocompetent people. The clinical spectrum varies depending on the degree of immunocompromise, ranging from colonization to invasive disease, with possible involvement of the lungs, sinuses, brain, and skin. Invasive pulmonary aspergillosis has a nonspecific presentation, with cough, pleuritic chest pain, and fever. A high index of suspicion is required for early diagnosis.[20] Aspergilloma forms in preexisting lung cavities, commonly secondary to tuberculosis, and is usually asymptomatic.[21]

Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity reaction to bronchial colonization by Aspergillus fumigatus. Patients usually have a prior diagnosis of atopy, asthma or cystic fibrosis.[22] Presents as asthma complicated by bronchial obstruction, fever, malaise, expectoration of brownish mucus plugs, peripheral blood eosinophilia, and hemoptysis. Untreated, ABPA can lead to bronchiectasis, fibrosis, and respiratory compromise.

Aspiration is the inhalation of foreign material into the airways beyond the vocal cords.[23] It can be categorized as aspiration pneumonitis or aspiration pneumonia. Aspiration pneumonitis is chemical injury after aspiration of gastric contents.[24] Strong risk factors include a decreased level of consciousness of any cause, which may lead to inadequate cough reflex and impaired glottal closure; dysphagia; general anesthesia; intubation or tracheostomy tube; and older age.[25]

Aspiration pneumonia results from the inhalation of oropharyngeal contents into the lower airways that leads to chemical pneumonitis, lung injury, and resultant bacterial infection. It commonly occurs in patients with altered mental status who have an impaired gag or swallowing reflex.[26] Diagnosed based on clinical signs or symptoms of pneumonia (e.g., cough, breathlessness, fever) and a history of, or risk factors for, aspiration.

Neonatal pneumonia may result from aspiration, often of meconium, which causes an inflammatory reaction in the airways. Infants born through meconium-stained amniotic fluid are at risk and typically present with respiratory distress soon after birth.[27]

Bronchiolitis obliterans organizing pneumonia (BOOP), is an inflammatory disorder of the distal bronchioles and alveoli.[28]It has distinctive radiographic findings, histological features, and response to corticosteroids (unlike usual interstitial pneumonia). The most common type is idiopathic BOOP; other types include focal nodular, post-infection, drug-related, rheumatological, immunological, organ transplantation, radiotherapy, environmental, and miscellaneous BOOP. In most cases the etiology is unknown; the term cryptogenic organizing pneumonia (COP) may be applied in these cases. COP refers to an organized inflammatory process in the alveoli from an unknown cause.[29] 

Hypersensitivity pneumonitis (HP), also known as extrinsic allergic alveolitis, is the result of non-IgE mediated immunologic inflammation. HP is caused by repeated inhalation of nonhuman protein, which can be of natural plant or animal origin or can be the result of a chemical conjugated to a human airway protein, such as albumin. The inflammation of HP manifests itself in the alveoli and distal bronchioles. Recent ATS/JRS/ALAT diagnostic guidelines classify patients as having fibrotic or non-fibrotic HP. Classification is determined by the predominant presence or absence of fibrosis on radiographic and/or histopathologic examination.[30] Many cases of HP are caused by occupational exposure.[31] 

Dyspnea, also known as shortness of breath or breathlessness, is a subjective sensation of breathing discomfort. The etiology is broad, ranging from mild, self-limiting processes to life-threatening conditions. Diseases of the cardiovascular, pulmonary, and neuromuscular systems are the most common etiologies. The differential diagnosis can be narrowed by making a distinction between acute, subacute, and chronic dyspnea, which is present for over 4 weeks.[32] Dyspnea is a key diagnostic feature of pneumonia.

Cough is a common respiratory symptom, which can pose a diagnostic challenge because of its association with a range of conditions.[33] Cough can be classified according to its duration. An acute cough lasts less than 3 weeks and is most commonly due to a viral upper respiratory tract infection. Subacute cough lasts between 3 and 8 weeks and is usually postinfectious in origin.[34] Common etiologies of chronic cough (cough persisting for >8 weeks) in nonsmoking adults, with a normal chest x-ray, who do not take ACE inhibitors, include upper airway cough syndrome; asthma; gastroesophageal reflux disease; and nonasthmatic eosinophilic bronchitis.[35][36] Patients with chronic cough (usually productive of sputum), a history of fever, malaise, and chest pain, and exam findings of dullness to percussion, decreased breath sounds, and presence of rales, should be tested for pneumonia.

Persistent pulmonary infiltrate results when a substance denser than air (e.g., pus, edema, blood, surfactant, protein, or cells) lingers within the lung parenchyma. Nonresolving and slowly resolving pneumonias are the most common broad categories of persistent pulmonary infiltrate.[37] Persistence is attributed to defects in host immune defense mechanisms, presence of unusual or resistant organisms, or diseases that mimic pneumonia.[38]

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