Last reviewed:September 2019
Last updated:October  2019

Introduction

Related conditions

Condition
Description

Community-acquired pneumonia (CAP) is defined as pneumonia acquired outside hospital or healthcare facilities. Older patients in particular are often afebrile and may present with confusion and worsening of underlying diseases. The most common cause is Streptococcus pneumoniae (also known as pneumococcus), which is considered to be the prototype of typical bacterial pneumonia. Mycoplasma pneumoniae is also a major cause and is considered to be the prototype of atypical bacterial pneumonia.[1] Bacterial and viral pathogens are the leading cause of CAP. Fungal and parasitic infections occur less commonly, but should be considered in immunocompromised patients or those with a relevant travel history, respectively.

Hospital-acquired pneumonia (HAP) is an acute lower respiratory tract infection that is by definition acquired after at least 48 hours of admission to hospital and is not incubating at the time of admission. 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 most recent guidelines for HAP and VAP by the Infectious Diseases Society and the American Thoracic Society.[2] HAP and VAP are usually due to bacterial infection, and the timely initiation of appropriate antimicrobial therapy is a key prognostic factor.[3] A lower respiratory tract culture should be obtained before initiating antibiotics, and the results used to de-escalate therapy and target the specific pathogen. Broad-spectrum agents are indicated where there are risk factors for multi-drug-resistant pathogens.[4]

Viral pneumonia

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.[5] 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 non-specific, but a diagnosis can be made by isolating viral nucleic acid from respiratory tract secretions.[6] There are a number of effective antiviral therapies and prophylactic measures for specific viral infections, which may be offered to patients at high risk. However, supportive care remains the cornerstone of treatment in the general population.[7] Co-infection 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]

Severe acute respiratory syndrome (SARS) is a viral pneumonia caused by the SARS coronavirus (SARS-CoV).[9] Risk factors include a history of recent travel, close contact with infected individuals, and laboratory work with SARS-CoV. Patients initially develop influenza-like prodromal symptoms. Cough (initially dry), dyspnoea, and diarrhoea may be present in the first week, but are more commonly reported in the second week of illness. Transmission occurs mainly during the second week of illness.[10] In severe cases, patients develop rapidly progressing respiratory distress and oxygen de-saturation, with about 20% requiring intensive care.[11][12][13][14]

Middle East respiratory syndrome (MERS) is an acute viral respiratory tract infection caused by the novel betacoronavirus Middle East respiratory syndrome coronavirus (MERS-CoV). MERS should be considered when a severe respiratory illness occurs in the 2 weeks following residence in or travel to the Middle East or areas of outbreak, and/or close contact with infected individuals. The majority of cases are the result of human-to-human transmission with peaks of confirmed cases occurring during nosocomial outbreaks.[15] The clinical spectrum of infection varies from no symptoms, or mild respiratory symptoms, to severe, rapidly progressive pneumonia, acute respiratory distress syndrome, septic shock, or multi-organ failure resulting in death. Treatment is mainly supportive.

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 (Chlamydia pneumoniae), and Legionella pneumophila.[16] Atypical bacterial pneumonia is usually characterised 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. As a cohort, patients who are hospitalised with atypical infection tend to be younger, and are less likely to have cardiovascular, renal, or metabolic comorbidities, than those with non-atypical pneumonia.[17]

Mycoplasma pneumoniae causes community-acquired pneumonia and upper respiratory tract infection. 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).[16]

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.[18] The clinical features are non-specific and wide-ranging, but classically include a fever and cough, preceded by upper respiratory tract symptoms.[19] Pneumonia due to C pneumoniae cannot be differentiated clinically from other atypical pneumonia-causing organisms, especially Mycoplasma pneumoniae.[20]

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.[21] 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 diarrhoea. Legionella pneumophila infection may result in a severe pneumonia, necessitating intensive care unit admission.[22]

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-positive patients with CD4 cell counts <200 cells/microlitre, recipients of bone marrow or solid-organ transplants, or patients receiving chronic immunosuppressive therapy or long-term corticosteroids.

Coccidioidomycosis is a fungal infection caused by the endemic fungus Coccidioides species, found within the endemic areas of the southwest US, northern Mexico, and limited areas of Central and Southern America. Infection is acquired through the inhalation of airborne arthrospores, and may be asymptomatic, or be the cause of acute and chronic pulmonary syndromes, and, rarely, extrapulmonary infection.[23]

Aspergillosis is an infection caused by inhalation of the aerosolised conidia (spores) of the Aspergillus fungus, which is found ubiquitously in soil. Aspergillosis mostly affects immunocompromised patients and is rare in immunocompetent hosts. The clinical spectrum varies depending on the degree of immunocompromise, ranging from colonisation to invasive disease, with possible involvement of the lungs, sinuses, brain, and skin. Invasive pulmonary aspergillosis has a non-specific presentation, with cough, pleuritic chest pain, and fever. Notably, fever may be absent in immunocompromised patients, and a high index of suspicion is required for early diagnosis.[24] An aspergilloma forms in pre-existing lung cavities, commonly secondary to tuberculosis, and is usually asymptomatic.[25]

Aspiration is the inhalation of foreign material into the airways beyond the vocal cords.[26] It can be categorised as aspiration pneumonitis or aspiration pneumonia. Aspiration pneumonitis is chemical injury after aspiration of gastric contents.[27] 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 anaesthesia; intubation or tracheostomy tube; and older age.[28]

Aspiration pneumonia results from the inhalation of colonised oropharyngeal contents into the lower airways. Key diagnostic features include cough and dyspnoea in the context of risk factors for aspiration, which should prompt referral for a swallow assessment.[29]

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.[30]

Bronchiolitis obliterans organising pneumonia (BOOP), more recently termed cryptogenic organising pneumonia, is an inflammatory disorder of the distal bronchioles and alveoli.[31] The typical presentation is an individual with a flu-like illness that develops over a few weeks, consisting of a mild fever, arthralgia, fatigue, and a non-productive cough. In most cases the aetiology is unknown; however, organising pneumonia can arise following infectious pneumonia, exposure to specific medications or environmental triggers, post-organ transplantation, or in the context of immunological disease.[31] Shortness of breath develops later and bilateral end-inspiratory crackles are often heard on examination. Most patients respond well to treatment with corticosteroids.[31]

Hypersensitivity pneumonitis (HP), also known as extrinsic allergic alveolitis, is the result of non-IgE mediated allergic reaction, in response to repeated inhalation of allergens. These include a range of organic materials or low molecular weight chemicals and metals, present in the workplace.[32] The inflammation of HP manifests itself in the alveoli and distal bronchioles. The clinical features depend on the concentration and frequency of exposure, with acute, chronic, and acute-on-chronic presentations described.[33]

Dyspnoea, also known as shortness of breath or breathlessness, is a subjective sensation of breathing discomfort. The aetiology is broad, ranging from mild, self-limiting processes to life-threatening conditions. Diseases of the cardiovascular, pulmonary, and neuromuscular systems are the most common aetiologies. By making a distinction between acute dyspnoea and chronic dyspnoea, which is present for over 4 weeks, the differential diagnosis may be narrowed.[34] Dyspnoea 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.[35] 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 post-infectious in origin.[36] Once cough duration has exceeded 8 weeks, a systematic approach to elucidating the cause and best treatment is needed. Common aetiologies of chronic cough (cough persisting for >8 weeks) in non-smoking adults, with a normal chest x-ray, who do not take ACE inhibitors, include upper airway cough syndrome; asthma; gastro-oesophageal reflux disease; and non-asthmatic eosinophilic bronchitis.[37][38] Patients with chronic cough (usually productive of sputum), a history of fever, malaise, and chest pain, and examination 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, oedema, blood, surfactant, protein, or cells) lingers within the lung parenchyma. Non-resolving and slowly resolving pneumonias are the most common broad categories of persistent pulmonary infiltrate.[39] Persistence is attributed to defects in host immune defence mechanisms, presence of unusual or resistant organisms, or diseases that mimic pneumonia.[1]

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