Streptococcus pneumoniae (the pneumococcus) is the most common causative pathogen of CAP across a range of severities and patient ages. However, other studies have found that influenza virus is the most common cause of CAP in adults. In Europe and the US, S pneumoniae accounts for about 30% to 35% of cases. Other bacterial causes include Haemophilus influenzae, Staphylococcus aureus (including MRSA), group A streptococci, and Legionella spp. For example, Legionella pneumophila (especially serogroup 1) accounts for 2% to 6% of CAP in immunocompetent patients.
Atypical bacteria are also common causes, although they vary in frequency depending on the year and any epidemics. The incidence of atypical pathogens in community-acquired pneumonia is approximately 22% globally, but this varies with location. Commonly reported atypical bacteria include Mycoplasma pneumoniae, Chlamydophila pneumoniae, Chlamydia psittaci and Coxiella burnetii. These pathogens are difficult to diagnose early in the illness and are sensitive to antibiotics other than beta-lactams (e.g., macrolides, tetracyclines or fluoroquinolones).
M pneumoniae accounts for up to 37% of CAP patients treated as outpatients and 10% of patients who are hospitalised. C pneumoniae accounts for 5% to 15% of cases of CAP. However, a Dutch study identified C psittaci by polymerase chain reaction (PCR) of sputum (when available) as a cause of CAP in 4.8% of cases. One German study identified C burnetii by PCR and/or antibody detection as the cause of CAP in 3.5% of patients.
Pseudomonas aeruginosa may also be prevalent in patients with pneumonia, depending on the region; however, it is more common in hospital-acquired and ventilator-associated pneumonia compared with CAP. It accounted for 7.7% of all isolates in CAP in a systematic review in China.
Respiratory viruses are reported in about 10% to 30% of immunocompetent adults hospitalised with CAP. Influenza virus A/B, respiratory syncytial virus, adenovirus, rhinovirus, and parainfluenza virus are the most common viral causes of CAP in immunocompetent adults. Newer pathogens reported to cause CAP include metapneumovirus and coronaviruses. Detection of viral causes is increasing because of the use of PCR.
Pneumonia develops subsequent to the invasion and overgrowth of a pathogenic micro-organism in the lung parenchyma, which overwhelms host defences and produces intra-alveolar exudates.
The development and severity of pneumonia is a balance between pathogen factors (virulence, inoculum size) and host factors. The likely microbial causes of CAP differ according to a number of factors, including differences in local epidemiology, the setting (outpatients, hospitalised, or intensive care unit), severity of disease, and patient characteristics (e.g., sex, age, and comorbidities).
Microbes that are present in the upper airways can enter the lower airways by microaspiration. Nevertheless, the defence mechanisms of the lungs (innate and acquired) keep the lower airways sterile. The development of pneumonia indicates a defect in host defences, exposure to a particularly virulent micro-organism, or a large inoculum size.
Impaired immune response (e.g., caused by HIV infection or advanced age) or dysfunction of defence mechanism (e.g., through current or passive smoking, COPD, or aspiration) leads to greater susceptibility to respiratory infections in patients.
Pathogens can reach the lower respiratory tract by 4 mechanisms:
Inhalation, a common route of entry for viral and atypical pneumonia in younger healthy patients. Infectious aerosols are inhaled into the respiratory tract of a susceptible person to initiate infection
Aspiration of oropharyngeal secretions into the trachea, the primary route through which pathogens enter the lower airways
Haematogenous spread from a localised infected site (e.g., right-sided endocarditis)
Direct extension from adjacent infected foci (e.g., tuberculosis can spread contiguously from the lymph nodes to the pericardium or the lung, albeit rarely).
There is a new theory that CAP may result from dysbiosis of the normal lung flora, rather than invasion of pathogenic micro-organisms in a sterile environment; however, this model requires further research.
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