Community-acquired pneumonia (CAP) is a frequent lower respiratory tract infection.

It is highly influenced by the geographic area and the population.

The microorganisms may reach the lower respiratory tract from inhaled air or from infected oropharyngeal secretions (Vincent et al. 1995). Droplet transmission from human to human is another usual mode of spread of the pulmonary infection, especially in immunocompetent patients and young children.

Clearance by mucociliary system can filter infective organisms 5–10 nm in diameter, so that microorganisms between 1 and 2 nm can reach the alveolar tissue. The alveolar infection depends on the balance between the virulence of the microorganism and body defenses due to cellular phagocytosis. There are several factors predisposing to the development of CAP as cardiovascular diseases, diabetes, uremia, immunodeficiency, obstructive pulmonary chronic disorders with mucociliary clearance insufficiency, and age.

Alcoholic patients and people with poor oral hygiene are particularly sensitive to develop pulmonary infections (Barlettand Finegold 1974).

The clinical presentation of pneumonia is frequently represented with sudden symptoms as high fever, cough, purulent expectoration, and deep chest pain. Neutrophilia is common.

CAP is classified into three main groups: lobar pneumonia, bronchopneumonia, and interstitial pneumonia (Bhalla and Mc Loud 1998).

Lobar pneumonia appears in the lung parenchyma periphery and then diffuses up to the hilum. It is generally limited to one pulmonary segment or lobe.

Bronchopneumonia occurs when infectious microorganisms produce acute bronchial mucosal inflammation and spread through the airway into the alveolar spaces determining pulmonary consolidation.

Interstitial pneumonia is determined by the infection of pulmonary interstitium and is mainly caused by viral organism.

The same organism may produce several different patterns that depend on the balance between the microorganism charge and the body immunity defenses.

The spectrum of bacteria responsible for CAP includes Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus, Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella pneumophila, and Klebsiella pneumoniae (American Thoracic Society 1995; Marom et al. 1999; De Paso 1991).

Haemophilus influenzae also is one of the most frequent bacteria causing CAP, because it frequently colonizes the human upper respiratory tract, especially the nasopharynx, and is considered to form part of the normal respiratory flora. It is also an important cause in the acute exacerbation of chronic obstructive pulmonary infectious disease (Kofteridis et al. 2009).

The viruses that most commonly cause pneumonia are respiratory syncytial virus, herpes simplex, parainfluenza virus, influenza virus, adenovirus, and cytomegalovirus.

The funguses that most commonly cause pneumonia are Pneumocystis, Aspergillus, and Candida.

Pulmonary emphysema and bronchiectasis are frequently seen in patients with CAP because chronic obstructive pulmonary disease is a predisposing factor for developing pulmonary infection (Reittner et al. 2000a) (Fig. 1).

Depending on the severity of the pulmonary alveolar tissue involvement, the pattern of the infection may be patchy or homogeneous. The consolidation is usually confined to one lobe, although multilobar involvement is not uncommon (Fig. 2). Because the bronchial tree is not involved, there is no volume loss of the inflamed pulmonary segment or lobe.

Lobar pneumonia is characterized by the filling of alveolar spaces by edema full of white and inflammatory cells. The inflammation generally begins at the lung mantle and then diffuses to the entire lobe through Kohn pores and peripheral small airways; usually it is limited by an interlobar fissure. The air bronchograms within the consolidation area are preserved (Fig. 2). Nodular pneumonia is frequently caused by fungal infections and is prevalent in young or immunocompromised patients.

The pneumonia could be complicated with cavitation and abscess (Fig. 3), necrosis of the inflamed lung parenchyma, and loculated empyema (Muller et al. 2007).

Abscesses develop in up to 30 % of cases, are usually solitary, and typically have an irregular wall. They could rupture into the pleural space with the development of pneumothorax and empyemas (Fig. 4). Abscesses may also erode into bronchial tree and produce air-containing cavities with fluid levels. The consequent bronchial aspiration and diffusion of infection can determine patchy consolidation or nodules in dependent portions of both the lungs (Fig. 5). The consolidations are usually multilobar and bilateral in distribution.

A large solitary abscess or primary lung abscess can develop in a patient without underlying lung inflammation as a consequence of aspiration of oropharyngeal secretions in combination with impairment of systemic defense condition.

Necrotizing pneumonia, generally determined by Gram-negative bacteria, produces exfoliated pulmonary tissue within a cavity or diffuses microabscesses secondary to thrombosis of the vessel that supply the consolidation. Sometimes necrotizing pneumonia consists of a fulminant process associated with focal areas of necrosis that results in abscesses that can coalescence, resulting in large cavities that may exhibit thick fibrotic walls if they are chronic. There are large cavities with concomitant small cavities frequently associated with empyema (Winer-Muram et al. 1993). This feature is frequent in immunocompromised patients.

Bronchopneumonia or lobular pneumonia is characterized by a peribronchiolar inflammation with thickening of peripheral bronchial wall, the diffusion of inflammation to the centrilobular alveolar spaces, and development of nodules (Fig. 6). From the centrilobular tissue, the inflammation can spread to lobular (Fig. 7) or subsegmental areas giving a consolidation. The areas of consolidation may be patchy or confluent, multilobar, unilateral, or bilateral (Fig. 8). Because the process involves the airways, it can determine a loss of volume of the affected pulmonary segment (Ito et al. 2009).

Interstitial pneumonia is frequently caused by virus.

The viral pneumonia begins with the destruction and exfoliation of the respiratory ciliated and mucous cells. The interstitial septa and the bronchial and bronchiolar walls become thickened for the inflammation process and lymphocyte interstitial infiltrates (Fig. 9). The consequent interstitial pneumonia has often a patchy appearance, frequently with coalescence, involving predominantly the peribronchial portions of the pulmonary lobules (Shiley et al. 2010). With the progression of inflammation, the alveolar sacs fill with exudate that could be hemorrhagic. As consequence a hyaline membrane can develop in alveolar spaces.

The pneumonia can heal completely, but sometimes a chronic interstitial fibrosis can occur.

Chest radiography represents an important initial examination in all patients suspected of having pulmonary infection and for monitoring response to therapy.

Its role is to identify the pulmonary opacities (Fig. 10), their internal characteristics and distribution, pleural effusion, and presence of other complications as abscesses and pneumothorax.

Radiographic manifestations depend on the immune status of the patient and the presence of preexisting lung chronic alterations as emphysema, chronic bronchitis, and bronchiectasis and vary somewhat among the various species of causing microorganisms.

The most common radiographic findings include hazy ground-glass opacities, confluent or patchy airspace consolidations, cavitations, and poorly defined linear or reticular-nodular opacities (Chastre et al. 1998).

These alterations may involve mainly the perihilar regions, lower lung zones, or upper lung zones. They are usually unilateral but may involve both lungs. Other findings are pleural effusion and hilar adenopathy.

In some cases, the radiographic findings are suggestive or consistent with the diagnosis of pneumonia and are sufficiently specific in proper clinical context to preclude the need for additional imaging (Fig. 11) (Franquet 2001).

However, the bedside plain film, the projection effects, and the poor density resolution frequently limit the value of radiography as a diagnostic tool. Radiographic features are sometimes nonspecific, and the relatively low diagnostic accuracy of chest radiography can be improved with CT.

CT has been shown to be more sensitive than x-ray plain film and provide additional information that affects diagnosis or management in up to 70 % critically ill patients (Heussel et al. 1997).

High resolution CT allows accurate assessment of airspace inflammation (Okada et al. 2012).

The distribution of parenchymal alterations is based on the evidence of their localization at CT scan. If the primary opacity is predominantly located in the inner third of the lungs, the pathology is classified as having a central distribution. A peripheral opacity is defined as a lesion localized in the outer third of the lungs. Zonal predominance is classified as either upper or lower. In the upper lung zone predominance, the alteration is located above the level of the tracheal carina, whereas in the lower zone predominance, it is located below the upper zone.

The CT findings include nodules, interlobular septal thickening, intralobular reticular opacities, ground-glass opacities, tree-in-bud pattern, lobar-segmental consolidation, lobular consolidation, abscesses, pneumatocele, pleural effusion, pericardial effusion, mediastinal and hilar lymphadenopathies, airway dilatation, and emphysema.

Nodules measure from 3 to 10 mm and are divided into three types: centrilobular nodules that are small nodules in centrilobular location, peribronchovascular nodules that are relatively larger nodules associated with the peribronchovascular bundle, and “random nodules” that are not associated with centrilobular structures or bronchovascular bundle.

The centrilobular nodules reflect a peribronchial inflammation with a centrilobular distribution (Fig. 12).

They are defined as a dot-like opacities localized inside the center of a secondary pulmonary lobule. They are present around the peripheral pulmonary arterial branches or 3–5 mm from the pleura, interlobular septa, or pulmonary veins.

Nodules that are present in the bronchovascular bundle are called peribronchovascular nodules (Fig. 13).

Hemorrhagic pulmonary nodules have a central area of soft tissue attenuation surrounded by a halo of ground-glass attenuation (Primack et al. 1994).

Pulmonary hemorrhage in association with nodules occurs in patients with herpes simplex virus, candidiasis, and cytomegalovirus pneumonia (Thurlbeck et al. 1991)

Interlobular septal thickening are defined as abnormal widening of the interlobular septa. Intralobular reticular opacity is considered to be present when interlacing line shadows are separated by a few millimeters (Fig. 9) (Austin et al. 1996).

It is frequently associated with bronchial wall thickening. Thickening of the bronchovascular structures is defined as an apparent thickening of the bronchovascular bundle in comparison with the unaffected lung parenchyma (Fig. 14).

Ground-glass opacity was defined as hazy increased opacity with preservation of bronchial and vascular markings (Fig. 15). It is present particularly in pneumocystis and cytomegalovirus infections (Fig. 16).

Tree-in-bud pattern may be seen in a variety of bacterial, mycobacterial, fungal, and viral infections and consists of centrilobular branching tubular structures, bronchovascular bundle thickening, and nodules and reflects the presence of bronchiolar inflammation and filling of the bronchiolar lumen by inflammatory exudate (Fig. 17) (Aquino et al. 1996).

Airspace consolidation is considered to be present when homogeneous increases in pulmonary parenchymal attenuation obscured the margins of vessels and airway walls (Fig. 2) (Hansell et al. 2008).

The CT findings in viral pneumonia are based on the evidence of small patchy opacities that can coalescence (Fig. 18), composed of multiple, poorly defined 2–3 mm nodules; multilobar involvement is frequent. Bronchial wall and peribronchial thickening frequently spread outward from the hila. Hilar adenopathy and pleural effusion are common.

The abscess can drain into a bronchus that leads to the classic air-fluid level, present in up to 72 % of cases (Fig. 3). The complete drainage of the cavity can lead to a pneumatocele.

Pneumatocele is a frequent consequence of an abscess drained in the lumen of a bronchus; it is a gas-filled area with a thin wall that may increase and can get ruptured into the pleural space, causing a pneumothorax. It can also heal completely, fading from the periphery to form a tiny thin-walled air-cyst or a linear scar.

Pleural effusion is better detected with CT than with radiography and is often associated with a high risk of empyema that requires prompt early drainage.

Purulent pericarditis is a relatively rare and a rapidly fatal complication of pneumonia. The consequent development of cardiac tamponade may be rapid. At the beginning, heart size may be normal at chest radiograph, whereas CT can demonstrate early the pericardial effusion that requires prompt drainage for avoiding cardiac compression (Fig. 19) (Naidich et al. 1983).

Mediastinal and hilar lymphadenopathies are evaluated when the minimal diameter of a lymph node is larger than 10 mm. Lymph node enlargement is very frequent in pneumonia and generally involves the paratracheal, tracheobronchial, and subcarinal mediastinal chains.

Airway dilatation predisposes to pneumonia and is considered to be present if the bronchial size exceeded that of the near pulmonary artery.

Pulmonary emphysema is frequently associated with pneumonia and is defined as scattered or diffuse areas of low attenuation without internal vascular structures in comparison with normal pulmonary parenchyma (Fig. 1).

Pneumonia is the first leading cause of death due to infection worldwide (Vilar et al. 2004a).

Many Gram-positive, Gram-negative bacteria, funguses, and viruses can cause the infectious pulmonary disease, and the severity of pneumonia depends on the balance between the microorganism charge, the body immunity defenses, and the quality of the underlying pulmonary tissue.

Among the types of CAP, S. pneumoniae is the most frequent causing bacteria, has a tendency to develop antibiotic resistance, and is associated with a high mortality rate in the elderly and childhood (Musher et al. 2002).

Radiographically pneumonia is divided into three patterns: lobar pneumonia, bronchopneumonia, and interstitial pneumonia (Muller et al. 2007).

Chest x-ray film is routinely performed for the initial evaluation of patients with suspect pulmonary infection, and it is considered the recommended tool for the diagnosis of CAP. However, chest x-ray film not always evidences all the findings of pneumonia, and it is limited by the interobserver variability in interpretation.

Especially in not clear or even negative chest radiography pattern, in patients with clinical symptoms, CT is recommended, for its high spatial resolution and the ability to evidence very early and minimal pulmonary alterations indicative of pneumonia.

Community-acquired pneumonias have been traditionally divided into “typical” and “atypical” pneumonias. The main aim of such a classification was to help the clinician narrow the differential diagnosis and choose an appropriate therapy based on the likely offending organism (Murray and Mason 2010).

Typical pneumonia is characterized by infection with bacteria such as Streptococcus pneumoniae, Klebsiella pneumoniae, and Haemophilus influenzae. It presents with symptoms such as acute onset of high grade fever with chills, cough with purulent expectoration, and pleuritic chest pain. Further evaluation of these patients reveals an elevated white blood cell count, elevated CRP, and lobar or segmental consolidation on imaging studies (Murray and Mason 2010).

Atypical pneumonia, as the name explains, does not show these typical features. An early use of this term in the literature dates back to 1938 when cases of patients who presented with milder symptoms and protracted course came to notice (Reimann 1938). These patients had more generalized symptoms like malaise, body pains, and low-grade fever with dry cough and flu-like symptoms. The causative organism could not be cultivated on regular media or stained with regular staining methods. Mycoplasma was first isolated in 1944 and was attributed as the etiology of primary atypical pneumonia (Eaton et al. 1944). However, several other organisms cause atypical symptoms.

Although originally used to signify any infection that was unusual in presentation, atypical pneumonia is now a broad term that includes infections caused by common organisms like Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella pneumophila and viruses (Marrie et al. 1981). Atypical, however, does not mean that they are rare; they account for almost 15–20 % of the cases of CAP (Arnold et al. 2007). Mycoplasma pneumoniae is the most common cause of atypical pneumonia followed by Chlamydia pneumoniae and Legionella pneumophila (Arnold et al. 2007). Apart from these conventional pathogens, there are emerging infections with newer organisms like Hantavirus, human metapneumovirus that can also cause atypical pneumonia. In view of the current radiological discussion and similar radiological appearances shared by mycoplasma and various viruses, we will also be discussing some additional infections in this chapter, which, although not considered routinely under the heading of “atypical pneumonia,” are atypical enough to justify their inclusion here.

Infections with many, if not all, atypical organisms share some common features. Mycoplasma, chlamydia, and viruses have many similarities in their pathology, clinical, and radiological features. Grossly, these pathogens cause predominant histological changes in the respiratory epithelium and in the peribronchial interstitium (Müller et al. 2007; Müller 2003). The ensuing bronchiolitis and alveolitis are characterized by infiltration of the epithelium with mononuclear cells and presence of neutrophilic exudate in the lumen of the airways. These changes are predominantly seen in the terminal and respiratory bronchioles and manifest radiologically as peribronchial nodules (Müller et al. 2007; Müller 2003).

Bronchiolitis with exudate in the lumen of the airways is seen on radiographs as reticulonodular pattern and on CT as tree-in-bud nodules. As the nodules enlarge, they involve the entire secondary pulmonary lobule and are seen as “lobular” consolidation: these features are typical of bronchopneumonia pattern. Further extension into segmental and patchy lobar consolidation may be seen in advanced stages, and this may be difficult to distinguish from bacterial infection. Partial filling of the airways gives rise to ground-glass opacities (Müller et al. 2007).

Some infections like influenza and hantavirus cardiopulmonary syndrome, on the other hand, cause rapidly progressive pneumonia with diffuse alveolar damage (Kim et al. 2002).

The clinical course of atypical pneumonias is generally subacute, the WBC counts are generally normal, and the imaging features are heterogeneous and nonspecific.

Diagnosis of pneumonia requires a combination of clinical, microbiological, and radiological features. Chest radiograph is usually sufficient to confirm the diagnosis. It also helps in follow-up of the patients and evaluation of the response to treatment. CT scans are not routinely recommended but are helpful in case of doubtful features on chest radiographs, when no adequate response to the treatment is noted and when complications or underlying pathology is suspected (Vilar et al. 2004b). CT scan can be further helpful in suggesting an etiological diagnosis. In indeterminate cases, CT-guided procedures come in as problem-solving tools for the correct diagnosis.

Lower respiratory tract infections can be caused by various viruses, and it is estimated that approximately 10 % of infections in CAP are due to viral etiology (ref). Along with the various radiological features, knowledge of the clinical history can be invaluable in narrowing the differential diagnosis. For example, in immunocompetent host, influenza virus is commonly implicated as an offender. In immunosuppressed individuals, however, the usual inciting organisms are herpes, cytomegalovirus, and adenovirus (Kim et al. 2002).

Viruses can be divided into (a) RNA viruses, myxoviruses (influenza, RSV, measles), coronavirus, and hantavirus, and (b) DNA viruses, adenovirus and herpes group including CMV and varicella zoster.

Although radiography and CT can be helpful in excluding a CAP, they may not be accurate in suggesting an etiological diagnosis. In every case, careful attention to the clinical history and radiological findings may help to narrow down the etiology and suggest the diagnosis.

Tuberculosis is often a challenge to the clinicians and radiologists alike, particularly in areas where it is not endemic. As the clinical signs and symptoms are often nonspecific, extra attention and a high degree of suspicion are required to make the right diagnosis.

As the manifestations of tuberculosis are a result of the interaction between the offending bacteria and the host immune system, there is no definite radiological picture that defines or is typical for tuberculosis and a wide range of differential diagnoses exist. However, some features, particularly when seen in typical distributions and typical combinations, can be very helpful in suggesting the right diagnosis, as discussed below.

Tuberculosis (TB) or captain of all these men of death is one of the oldest diseases known to mankind. It is still a disease of global concern, affecting millions of people worldwide every year. It is a leading cause of death among infectious diseases. Together with HIV, TB accounted for a staggering 1.5 million deaths in 2014 (World Health Organization 2015). Ninety-five percent of these deaths were reported in low- to middle-income countries, where tuberculosis is highly prevalent (World Health Organization 2015).

Although the incidence of TB globally has been showing a declining trend for several years, still an estimated 9.6 million new cases were reported by WHO in 2014. Majority of these cases were reported in Southeast Asia, Western Pacific, and Africa with highest number of incident cases seen in India, Indonesia, and Nigeria. 12 % of these patients were HIV positive, and notably 75 % of HIV-positive people with tuberculosis lived in Africa (World Health Organization 2015).

Europe accounts for 4 % of TB burden in the world with close to 1000 new cases per day (European Centre for Disease Prevention and Control 2015). Within the EU/EEA (European Union/European economic area), an overall declining trend in TB reporting in the last 10 years has been observed. It is noteworthy that a significant 28 % of cases were of foreign origin. In some countries like Luxemburg, Malta, Norway, Sweden, and Switzerland, the TB cases of foreign origin accounted for >70 % cases, highlighting the increased prevalence in migrants, with an increased prevalence of MDR-TB in these groups of patients (European Centre for Disease Prevention and Control 2015; Odone et al. 2015).