Etiology: The most common viral agents causing pulmonary infections in childhood are listed in Table 54-2.

Imaging: Bilateral interstitial opacities with peribronchial thickening and hyperinflation (see Fig. 54-1), thought to represent viral bronchiolitis, are nonspecific and are, in fact, indicative of an acute pulmonary infection of any cause (viral or bacterial) in young children.^1,15 Pleural effusions are rare in purely viral lung infections. Radiologic abnormalities often clear slowly and lag behind clinical improvement. Complications are superimposed bacterial infection (often hospital-acquired), and postinfectious bronchiolitis obliterans, bronchiectasis, or both.² These latter conditions, which frequently follow an adenovirus infection, are characterized by features of chronic air trapping and atelectasis resulting from bronchial dysfunction; mosaic perfusion abnormalities, peribronchial thickening, chronic atelectasis and bronchiectasis, best seen on computed tomography (CT).² Swyer-James-MacLeod syndrome is characterized by a unilateral small hyperlucent lung, which exhibits hypoperfusion and chronic bronchiectasis (e-Fig. 54-2).

In RSV infection, the lungs are often quite clear, or focal areas of superimposed atelectasis may be noted (see Fig. 54-1); when present, these predict a need for more prolonged mechanical ventilation.⁴⁰

In mild influenza infection, initial chest radiographs are normal or may demonstrate nonspecific prominence of peribronchial markings and hyperinflation. In children with a more severe clinical course, bilateral symmetric and multifocal areas of consolidation, often associated with ground-glass opacities, are seen (e-Fig. 54-3).⁴¹

The radiographic manifestations of SARS are typically mild, with interstitial thickening, which may progress to focal consolidation.42,43 In children, unlike in adults, no lymphadenopathy, pleural effusion, or cavitation is reported.⁴⁴ However, abnormalities may persist on thin-section CT in older children for up to 12 months following infection.⁴⁵

Measles virus is thought to be the cause of giant cell pneumonia, which produces a diffuse reticulonodular bronchopneumonia-like radiographic pattern (e-Fig. 54-4), with hilar node enlargement and superimposed bacterial infection, usually affecting the lower lobes. Atypical measles pneumonia following vaccination with, or exposure to, live virus was characterized by extensive nonsegmental parenchymal consolidation, with pulmonary nodules, hilar lymph node enlargement, and pleural effusion being common.

Adenovirus may cause necrotizing bronchopneumonia, bronchitis, or bronchiolitis. Radiographic features are nonspecific but usually include bronchial wall thickening, peribronchiolar densities, air trapping, and patchy or confluent consolidations.³⁰ Adenopathy is more common than in other viral pneumonias. Bronchiectasis or bronchiolitis obliterans may be a permanent sequel (see e-Fig. 54-2).^30,31,46

In children infected with CMV, often, a progressive interstitial pneumonitis is seen (e-Fig. 54-5). Gallium-67 scintigraphy may show abnormal uptake in the lungs of patients who have a normal chest CT.⁴⁷

Findings in varicella are similar to those of measles pneumonia. Multiple focal calcifications frequently develop after severe chickenpox pneumonia (e-Fig. 54-6).

In EBV infection, hilar and mediastinal lymph node enlargement may be seen (e-Fig. 54-7). Pulmonary involvement is uncommon but is characterized by bilateral reticular perihilar infitrates.⁴⁸

Treatment and Follow-up: Effective antiviral therapies have not been established, and treatment of viral pulmonary infections is mainly supportive. Experimental treatments to correct the acquired surfactant deficiency and dysfunction that occurs in critically ill infants with viral pulmonary infections are actively being investigated.³⁷ With a few exceptions, the use of extracorporeal membrane oxygenation to treat severe respiratory failure from ARDS, which frequently complicates severe infections, has not lead to better outcomes than that of optimal less invasive supportive care.³⁷ Certain high-risk infants may qualify for prophylactic injection of monoclonal antibodies against the F-glycoprotein of RSV. Since the most important complication of viral pulmonary infection is a superimposed bacterial infection, this should be actively looked for and treated with antibiotics when confirmed.²

Etiology: This organism is the most common cause of bacterial pneumonia in children less than 5 years of age. It is a gram-positive diplococcus, which infects healthy patients but also commonly attacks those with underlying illness, including the hospitalized and immunocompromised, and children with sickle cell anemia.⁵³ A strong association with a preceding viral infection, in particular influenza, is seen.⁵⁴ The virally activated respiratory epithelium has an increased expression of receptors for pneumococcal attachment.⁵⁵ In the usual case of an infected but otherwise healthy child, the onset is acute with fever, headache, and abdominal or chest pain. The pulse and respirations are rapid. By the second day, cough, expiratory grunts, rales, and pleural friction rub may be heard. Rapid clinical resolution usually occurs within 24 to 48 hours after treatment with antibiotics in patients with uncomplicated infections. However, a rapid increase has been seen in the incidence of partially or fully penicillin-resistant strains of S. pneumoniae.⁵⁶ Following the institution of conjugate pneumococcal vaccination, the proportion of children younger than 5 years with suspected occult pneumococcal pneumonia confirmed by radiography decreased from 15% to 9%.⁵⁷

Imaging: Pneumococcal pneumonia is usually confined to one lobe, but only rarely is the entire lobe consolidated. A pattern of homogeneous airspace consolidation is usual but not invariable, especially in the presence of underlying lung disease. This pneumonia may initially have a strikingly round appearance in children younger than 8 years (Fig. 54-8), simulating an intrapulmonary mass or abscess, until it spreads further to reach a normal anatomic boundary such as a fissure.^1,58,59 Pleural effusion, empyema (e-Fig. 54-9), and lung necrosis (e-Fig. 54-10) are infrequent complications, seen in less than 30% of patients. Resolution on radiographs is usually complete by 6 to 8 weeks.

Etiology: Group A streptococcus usually produces tonsillitis or pharyngitis. In the 1990s, S. pyogenes pneumonia, often associated with the toxic shock syndrome, was increasingly reported in childhood. It may occur de novo in a healthy child or follow a viral infection. In neonates, group B streptococcus is a leading cause of sepsis, including pneumonia and meningitis.

Imaging: Group A Streptococcus produces a bronchopneumonia in a segmental configuration with either homogeneous or patchy consolidation, which frequently affects a lower lobe. It may be bilateral. Pleural effusion and empyema are common in untreated cases. Lung abscess may be a complication. Clinically and on imaging studies, this pneumonia is very similar to staphylococcal pneumonia, although pneumatoceles are less commonly seen. Group B Streptococcus may accompany or mimic hyaline membrane disease in neonates, and is radiographically difficult to distinguish from it, although the presence of pleural effusion favors (concomitant) infection.

Etiology: This gram-positive, catalase-positive coccus primarily affects infants under the age of 1 year (70%). In debilitated patients, it occurs as a superinfection, particularly in the hospital. The incidence of “primary” staphylococcal pneumonia has decreased markedly since the early 1950s. However, staphylococcal pneumonia secondary to septicemia rather than inhalation of organisms is increasing and occurs in older children. This form of “embolic” disease may present with multiple nodular masses or abscesses (e-Fig. 54-11). This evolving pulmonary pattern in a child with sepsis should initiate a search for a distant source of infection, often in bones, joints, or skin.⁶⁰ Despite extensive pulmonary disease, if recovery occurs it is usually without sequelae. In comparison with methicillin-sensitive strains, methicillin-resistant strains of community-acquired S. aureus cause more serious pneumonias in younger children.^61,62

Imaging: In contrast to pneumococcal pneumonia, staphylococcal pneumonia is a lobular or bronchopneumonia, which begins in the airways rather than in the alveoli. Consolidation of peribronchiolar acinar units occurs initially in a segmental distribution. This infectious agent is very virulent, and severe hemorrhagic pulmonary edema may develop rapidly. Pneumatoceles are more common than in any other type (also reported in S. pneumoniae, H. influenzae, and Escherichia coli pneumonia) and occur in 40% to 60% of patients.61,63,64 They usually appear during the first week of the pneumonia and resolve within 3 months. Pneumatoceles often appear as the child is getting better, and their presence does not have prognostic significance. Ten percent of children with staphylococcal pneumonia have a pneumothorax, which may result from the rupture of a pneumatocele.^61,63,64 Pleural effusion and empyema are also very frequent, occurring in more than 90% of children (Fig. 54-12).⁶⁴

Etiology: Haemophilus influenzae is a gram-negative, rod-shaped bacterium, which was first discovered in 1892 during an influenza pandemic. In infants and young children, it causes bacteremia, pneumonia, cellulitis, epiglottitis, and meningitis. Since 1990, vaccination has markedly reduced the incidence of this pneumonia (<95%).

Imaging: The radiographic appearance is nonspecific: pulmonary opacities that often begin as a segmental, interstitial-appearing process progresses to airspace consolidation.⁶⁵ Approximately two thirds of cases have unilateral involvement, but more than one lobe is involved 25% of the time.⁶⁵ Empyema is a common complication, occurring in about 40%.⁶⁵

Etiology: Bordetella pertussis is a gram-negative, aerobic, capsulated coccobacillus. The incidence of pertussis (whooping cough) has decreased significantly with immunization, but it is still seen in young infants, particularly in the unimmunized. This agent is spread by airborne droplets. A characteristic clinical sign is the paroxysmal cough (whoop). Even after convalescence, the patient’s cough may persist for weeks or months. In China, the disease has been termed “the cough of 100 days.”

Imaging: Abnormal but nonspecific findings are present in most patients with pertussis. Because this is an airways-centered disease, it may mimic viral airways disease and pneumonia. The classic appearance is that of the “shaggy heart” (e-Fig. 54-13). However, nonspecific findings such as hyperaeration, atelectasis, segmental consolidations, and hilar lymphadenopathy are seen more commonly. Radiographic changes may persist for several weeks. Bronchiectasis may be a long-term complication.

Etiology: Pseudomonas aeruginosa is a gram-negative, aerobic, rod-shaped bacterium, which is an opportunistic pathogen in humans. Lungs, urinary tract, and kidneys are the common sites of infection. P. aeruginosa usually occurs as a nosocomial infection and is a major problem for patients with cystic fibrosis, in which thick layers of lung mucus and alginate produced by the bacteria may limit the diffusion of oxygen. Diagnosis of this infection depends on the Gram stain of sputum or other bacteriologic specimens (e.g., lung tissue, bronchoscopic aspiration, and bronchoalveolar lavage fluid).

Imaging: When the patient is infected by airway contamination, the process tends to involve both lung bases, with extensive bilateral parenchymal consolidation, patchy areas of disease with small abscess formation, or small regions of lobular emphysema. In the bacteremic form, widespread patchy or nodular shadows may be found throughout both lungs. Lung necrosis may also occur.

Etiology: Legionella pneumophila is an aerobic, pleomorphic, flagellated, gram-negative bacterium. It is the cause legionnaires’ disease, is mainly seen in immunocompromised patients and is rare in children.66,67

Imaging: Typically, initial radiographs show poorly marginated opacities that progress to more widespread consolidation, often accompanied by pleural effusion. Presentation as multiple pulmonary nodules has been reported but is less common.⁶⁷ Cavitation and abscess formation are complications.

Etiology: Anaerobic bacteria are uncommonly responsible for pneumonia and lung abscess.⁶⁸ Aspiration is the most common route of exposure, and Fusobacterium species, Bacteroides species, Peptococcus, and Peptostreptococcus may be cultured from the abscess or the pleural fluid.

Imaging: Usually, consolidation occurs in the lower respiratory tract, and clinical course is slowly progressive (e-Fig. 54-14). Lung abscess (e-Fig. 54-15) and fulminant necrotizing pneumonia may eventually develop.

Etiology: Chlamydia trachomatis is an intracellular bacterium commonly found in the genital tract, where it causes urethritis in men and cervicitis in women. In neonates, it causes conjunctivitis, which is contracted during passage through an infected birth canal. Chlamydia is a common cause of pneumonia in infants between 2 and 14 weeks of age.⁶⁹ The infant is affected by a staccato-like cough and may have conjunctivitis and eosinophilia, although these are not invariable findings. Usually, the patient is afebrile, with a radiographic appearance suggesting an illness more severe than the clinical findings indicate. Recently, C. pneumoniae has been recognized as a common agent causing community-acquired bronchitis and mild atypical pneumonia in school-age children.³ The clinical response to appropriate therapy is usually rapid.

Imaging: The radiographic findings of C. trachomatis infections are nonspecific (e-Fig. 54-16), but when they are analyzed in conjunction with clinical findings, the disease may be suspected. Bilateral involvement is usual.⁷⁰ The lungs are usually hyperaerated with increased linear density and patchy areas of consolidation, probably representing subsegmental atelectasis. Lobar consolidation is rare.⁷⁰

Etiology: This organism is one of the most common causes of pulmonary infection in childhood, accounting for 10% to 30% of pediatric pneumonias.⁷¹ It is most often seen in school-age children and is uncommon in children less than 3 years of age. It is acquired by droplet inhalation, and it is most commonly noted in families, in schools, and among military recruits. The disease is usually mild, with low-grade malaise, headache, fever, and cough. Stevens-Johnson syndrome (erythema multiforme) may complicate the disease. The diagnosis is established by culturing the organisms from sputum or by demonstration of rising specific Mycoplasma titers. A rise in the titer of cold agglutinins is seen in about 50% of cases but is nonspecific; of greater diagnostic value are immunofluorescent and complement fixation tests for specific antibodies and the recently developed molecular probes.⁷²

Imaging: This classic “atypical pneumonia” has a radiographic appearance that frequently mimics viral pulmonary infection (Fig. 54-17).¹ In early cases, a fine reticular pattern suggestive of interstitial inflammation may be seen.⁷³ This tends to be in a segmental distribution and in some cases progresses to airspace consolidation suggestive of bacterial pulmonary infection.^74,75 Small pleural effusions are seen in up to 20% of patients. Hilar adenopathy is common. Bilateral involvement occurs in approximately one third of cases. The radiographic changes are frequently more severe compared with the patient’s clinical condition. Resolution is often slow and lags behind clinical improvement.

Treatment and Follow-up: Treatment of bacterial pulmonary infections is with antibiotics and other chemotherapeutic agents, focused on the causative agent, either presumed (empirical treatment) or preferably directed by the results of culture or immunoassay. Complications of bacterial pulmonary infections are lung necrosis, abscess, empyema, and bronchopleural fistula.² Ultrasonography is the most effective initial cross-sectional modality when pleural complications are suspected, whereas CT is the preferred modality to diagnose parenchymal complications.^76–82 A review of the diagnostic performance of CT versus radiography confirms the expected higher sensitivity of CT.^78,83–90 CT is more sensitive than radiography to determine the cause of a delayed response to medical and percutaneous treatment of pediatric chest infections, but it is unclear whether this affects the eventual outcomes of treatment.^78,89 Cavitary lung necrosis is demonstrated well by CT.⁹⁰ However, most of the affected children recover without permanent sequelae on clinical and imaging follow-up.¹ For this reason, documentation of complete resolution of pneumonia in children who are otherwise healthy is not indicated.^1,22,91 CT and, potentially, magnetic resonance imaging (MRI) are helpful, however, to fully investigate any underlying focal anatomic cause such as anomalous bronchi, bronchogenic cysts, sequestrations, or bronchial atresia (Fig. 54-18), which may underlie recurrent or chronic pneumonia.^1,92–94 Conversely, the value of CT to monitor diffuse processes that predispose to repeated pulmonary infections such as chronic granulomatous disease of childhood and cystic fibrosis remains controversial.^95,96 Children with these chronic conditions will accumulate a substantial radiation burden from repeated examinations during their lifetime, and the theoretical risks of these procedures with regard to the induction of cancer will have to be balanced against the immediate clinical benefits, which remain unproven.⁹⁷ MRI has promise as a nonradiating cross-sectional imaging alternative for examination of these conditions.⁹²

Etiology: TB is caused by Mycobacterium tuberculosis, an aerobic, nonmotile, non–spore-forming rod. Although the resurgence of TB noted in the United States in the 1980s and 1990s has declined, in 2003, 15,000 new cases were reported, and the rate of decline appears to be slowing.⁹⁸ The incidence continues to increase worldwide.^99–101 Of all new cases of TB, 5% to 6% are in children less than 15 years of age, and approximately 60% of new childhood infections occur in children less than 5 years of age.⁹⁹ A significant number of new cases occur in immunocompromised patients, particularly in those with HIV infection.^102–104 The incidence of TB has decreased in the general population but has increased in the foreign-born population, accounting for 50% of new cases in the United States.

Inhalation of the tubercle bacillus is the most common route of infection in children. Congenital infection is extremely rare and is most often secondary to hematogenous spread across the placenta during pregnancy or from contaminated amniotic fluid. Pulmonary TB infection may be categorized into three groups: (1) primary infection; (2) miliary infection; and (3) reactive or postprimary infection.

The length of the incubation period of TB depends on the size of the initial inhaled inoculum and varies from 2 to 10 weeks; it ends when the patient becomes sensitized (i.e., has a positive skin test). Annual skin testing in high-risk groups is recommended. In the low-risk child, skin testing at 12 to 15 months, at 4 to 6 years, and in adolescence is a reasonable approach.¹⁰⁵ In asymptomatic primary tuberculosis, the disease is detected because of a routine skin test, and chest radiography is most often normal. In endemic areas, radiographs may demonstrate hilar lymphadenopathy only.^106–108 Because children produce little sputum, they do not transmit the disease to one another, and a search for the infected adult must be undertaken. The index child is always treated with antibiotics. Following this treatment, no evidence suggests that the few children with a positive skin test and abnormal findings on chest radiography have a clinical course or prognosis different from that of the majority of children with a positive skin test and normal chest radiographs.

If radiographs are positive, usually, a single small primary focus is present (70%), located in the subpleural region. From there, the bacilli spread through the lymphatics to regional hilar and mediastinal lymph nodes (primary complex, e-Fig. 54-19). In postobstructive tuberculosis, large lymph nodes may cause extrinsic bronchial compression, and granuloma formation may cause endobronchial obstruction, leading to segmental air trapping, atelectasis (e-Fig. 54-20), or both. The presence of airway obstruction in a child who does not appear to be sick may spuriously suggest the possibility of an inhaled foreign body.¹⁰⁹ For a few patients, bronchoscopy is required to diagnose the initial endobronchial lesion.¹¹⁰ Chronic obstruction may lead to bronchiectasis. Calcification occurs after caseation of the primary lesion and is seen earlier in infants (6 months after infection, e-Fig. 54-21) than in older children (2 to 3 years after infection, e-Fig. 54-22).

Progressive primary pulmonary tuberculosis is a serious but rare complication.¹¹¹ Progressive enlargement of the primary complex occurs, with caseation of the lesion followed by liquefaction (Fig. 54-23). The lesion may rupture into a bronchus, establishing new foci of disease (Fig. 54-24). Affected children are usually quite ill, with weight loss, dyspnea, anorexia, and failure to thrive. Pleural involvement in TB (e-Fig. 54-25) is usually noted in children older than 2 years, who present with fever, chest pain, and symptoms of pneumonia.¹¹² The pleural fluid usually has few organisms, many white cells, a high protein content, and a low glucose content.

The host response to lymphohematogenous spread is varied, with immunosuppressed patients being at greatest risk. A few children present with high spiking fevers, hepatomegaly, and positive blood culture (chronic tuberculous bacteremia, e-Fig. 54-26). Miliary tuberculosis usually occurs within 6 months of the primary infection and results from lymphohematogenous dissemination of M. tuberculosis from the primary complex (e-Fig. 54-27).

Reactivation or postprimary TB infection is the classic adult or adolescent form of the disease. It is the result of growth of previously dormant bacilli in the apices of the lung. The reactivated lesions in the apical and posterior segments of the upper lobes are composed of foci of caseous necrosis with surrounding edema, hemorrhage, and mononuclear cells. These lesions may liquefy and rupture into a bronchus, spreading the bacilli (e-Fig. 54-28). Cavitation with scarring occurs (Fig. 54-29). Reactivation of tuberculosis is rare in children who were infected with primary tuberculosis before the age of 2 years. It is much more frequent in children whose primary infection occurred after the age of 7 years, particularly if they were initially infected near puberty.⁹⁸

Imaging: Primary TB infection of the lung falls under the subcategory of subacute dense focal (atypical) pneumonia (see e-Fig. 54-19).^15,113–115 Chest radiography is insensitive to primary infection.^116,117 In children with a positive skin test, screening with only a frontal radiograph is sufficient in nonendemic areas, whereas in endemic areas the addition of the lateral radiograph is beneficial for improved detection of hilar lymphadenopathy.^106,118 Almost half (43%) of children diagnosed with tuberculous meningitis have normal chest radiographs.¹¹⁹ CT typically shows a subtle parenchymal opacity with associated lymph node enlargement. In a large study of children with TB, when initial chest radiography was positive, hilar and peritracheal lymphadenopathy was the most common finding, present in 92% of the cases.^102,104 Studies using CT confirm that infected patients frequently have abnormal lymph nodes (see e-Figs. 54-19 through 54-21), but 50% may not have nodes larger than 1 cm.¹²⁰ Affected nodes typically are large and of low density with rim enhancement and calcify later in the course of the disease. The adenopathy may be contralateral to the parenchymal disease in one third of patients. Chest radiography is most useful for following the course of disease in children with recent conversion to tuberculin sensitivity and for the early detection of miliary TB infection (see e-Fig. 54-27), which produces a “snowstorm” pattern in the lung, liver, and spleen.¹²¹ Occasionally, this may be present before there is overt clinical manifestation of the disease; as expected, CT is more sensitive than chest radiography.^99,100 Regression of abnormalities is slow and may require from 6 months to 2 years to resolve on radiography and up to 15 months on CT evaluation (see e-Fig. 54-21 and Fig. 54-29).^104,122

Treatment and Follow-up: TB is treated with a combination of antibiotics and chemotherapeutic agents to which the organism is sensitive.¹²³ Multidrug resistance to the regimens is an increasing problem worldwide, but strategies for effective treatment and reinforcing patient adherence have proven successful, even in the developing world.¹²³ Because of the limited sensitivity of radiography, cross-sectional imaging with CT, when locally available, is frequently helpful for patient management (see e-Figs. 54-19 and 21, Figs 54-23, and 54-24; and e-Figs. 54-26 and 54-28).^{100,103,110–112,121}

Etiology: Nontuberculous mycobacteria (NTM) are widely distributed in the environment and may produce infection in patients with normal immunity, although infection is significantly more frequent in patients with immunodeficiencies (particularly HIV infection) or with altered local defenses (e.g., in cystic fibrosis or ciliary dyskinesia). Although the signs and symptoms of NTM pulmonary infection are variable and nonspecific, affected pediatric patients usually present with chronic cough, fever, chills, night sweats, dyspnea on exertion, and weight loss. The diagnosis is based on clinical, radiographic, and bacteriologic criteria.

Imaging: Although the radiologic findings of pulmonary NTM disease are variable, depending on the presence or absence of underlying disease, typical findings include multiple nodules, consolidation, and cavitation. Mediastinal or hilar adenopathy similar to that of TB may be present (e-Fig. 54-30). NTM may also complicate or cause bronchiectasis.

Treatment and Follow-up: Successful treatment depends on tailoring drug treatment to the type of NTM cultured. Because NTM pulmonary infection could be indolent, long-term clinical and radiological study follow-up (months to years) may be required at relatively short intervals.

Etiology: Aspergillus species are a group of ubiquitous molds within the environment that may be cultured from a wide variety of soils, water sources, and decaying organic matter. Pulmonary infection is most often caused by Aspergillus fumigatus. Although pulmonary infection with Aspergillus species may take a variety of clinical courses and imaging appearances mainly depend on the affected patients’ immune status, it can be grouped into three main categories: (1) fungal ball, (2) allergic bronchopulmonary aspergillosis (ABPA), and (3) invasive aspergillosis.¹²⁴ A fungal ball or mycetoma typically grows saprophytically in immunocompetent children with a preexisting cavity often related to cystic fibrosis or postprimary TB. ABPA, characterized by a hypersensitivity response to Aspergillus antigens, typically develops in children with cystic fibrosis or asthma.¹²⁵ Invasive aspergillosis almost exclusively occurs in immunocompromised children with underlying neutropenia related to bone marrow or solid organ transplantations and others receiving systemic chemotherapy.¹²⁴ The organism may produce a bronchocentric or angiocentric lesion and is associated with a high morbidity and mortality.¹²⁶ A semi-invasive, less aggressive form of Aspergillus infection may be seen in patients with underlying lung disease or in mildly immunocompromised patients.¹²⁷

Imaging: A fungal ball typically appears on chest radiographs as an intracavitary mass within a thick-walled cavity usually located in an upper lobe, especially the apical segment (e-Fig. 54-31). CT shows a round or oval-shaped cavity containing a freely mobile soft tissue mass surrounded by a crescent of air (Monad sign).¹²⁸ The most common features of ABPA are mucoid impaction within bronchiectasis and segmental and lobar atelectasis. Such dilated bronchi filled with inspissated mucus often cause a homogeneous branching opacity referred to as the finger-in-glove sign. Invasive aspergillosis characteristically appears as one or a few nodular opacities randomly distributed throughout the lungs. Distinctive but nonspecific characteristics include the halo sign and the air crescent sign. The halo sign refers to an irregular ground-glass opacity surrounding a nodule of infection (Fig. 54-32). The indistinct halo probably represents hemorrhage in lung adjacent to the nodule, resulting from vascular invasion. The air crescent sign is an air collection that partially outlines a masslike lesion that represents a contracting nodule.¹²⁸ This sign is noted in well-established Aspergillus infections when the host’s defense mechanisms have partially recovered.

Treatment and Follow-up: The main treatment goal in children with pulmonary aspergillosis is to correct any underlying immune deficiency and to control the infection with antifungal medications such as voriconazole and liposomal amphotericin B.

Etiology: Histoplasmosis, caused by Histoplasma capsulatum, is common in many parts of the United States. Initial infection is similar to that of the primary tuberculous complex except that in histoplasmosis, large numbers of pulmonary foci are the rule. Histoplasmosis may be categorized into three phases: (1) acute infection, characterized by nonspecific respiratory symptoms that usually develop 12 to 14 days after initial exposure; (2) chronic infection, which may resemble TB; and (3) disseminated infection. The diagnosis of pulmonary histoplasmosis rests on the identification of antigen and the demonstration of Histoplasma-specific antibodies. Rapid diagnosis may be obtained from biopsy of the granulomas with special fungal stains. Histoplasma may be cultured from lavage or blood specimens, but cultures take a long time to grow and have a low sensitivity.

Imaging: Radiographic findings are similar to TB in all phases of these diseases, and in some cases, they resemble those in coccidioidomycosis (e-Fig. 54-33).¹²⁹ Approximately 95% of patients are asymptomatic during the initial infection, and thus the initial exudative phase of the disease is much less obvious radiographically compared with the sequelae of infection.¹²⁹ The first phase of the infection is characterized by single or multiple pulmonary nodules that are 1 to 3 cm in size, as well as mediastinal and hilar lymphadenopathy. Pulmonary nodules that have been present for more than a few months usually show central or dystrophic calcification. Calcified mediastinal and hilar lymph nodes are often seen in patients with calcified pulmonary nodules (e-Fig. 54-34). Sarcoidosis may exhibit similar adenopathy. Because treatment of sarcoidosis involves immunosuppression, histoplasmosis must be excluded, particularly in endemic areas. In children with chronic histoplasmosis, upper lobe consolidations simulating TB infection, sometimes associated with cavitation, may be present. Disseminated histoplasmosis has been observed in infancy, and the imaging findings are similar to those in miliary tuberculosis. Massive hepatosplenomegaly is common in disseminated cases. Granulomatous or calcified foci in the spleen are a frequent incidental finding in endemic regions and are almost diagnostic of disease exposure in an otherwise healthy patient. A rare but devastating result of chronic pulmonary histoplasmosis is mediastinal fibrosis, which may lead to pulmonary artery compression (see e-Fig. 54-33) and terminal pulmonary artery hypertension. It may also result in compression of the superior vena cava, esophagus, trachea, and bronchi.

Treatment and Follow-up: Treatment is merely supportive in asymptomatic and mild cases, but when disseminated histoplasmosis is present, a combination therapy of antifungal agents is given (itraconazole, amphotericin B).

Etiology: Coccidioidomycosis, caused by Coccidioides immitis or C. posadasi, is acquired by inhalation. Endemic areas in the United States include the semi-arid regions of California, Arizona, New Mexico, and western Texas. The infection is usually self-limiting, and affected children present with mild flulike illness, with fever, cough, headaches, rash, and myalgia. However, severe pulmonary infection may develop in immunocompromised children (particularly those with HIV infection). The diagnosis may be made by positive reaction to the coccidioidin skin test or by positive culture of the sputum or gastric washings.

Imaging: Radiographic examination during the early stages of disease usually shows lobar or segmental airspace consolidation and enlargement of the regional lymph nodes.¹³⁰ The pulmonary opacity of primary coccidioidomycosis is similar to that in primary tuberculosis (e-Fig. 54-35). It usually clears after a few weeks—its duration is usually much shorter than in tuberculosis—and residual calcified foci appear later within both the lung and lymph nodes. Small localized or large free pleural effusions may be visualized early.¹³¹ Although small, sharply defined, thin-walled pulmonary cavities are commonly noted in adults, they are uncommon in children.

Treatment and Follow-up: Affected children with mild symptoms often do not require treatment. However, immunocompromised children with progressive or disseminated disease are treated with a combination of antifungal agents (amphotericin B, fluconazole, itraconazole, or ketoconazole).

Etiology: Pneumocystis carinii, a unicellular organism, that infects humans, was recently renamed Pneumocystis jiroveci. Originally considered a parasite, it is currently categorized as a fungus on the basis of molecular similarities to fungal RNA. This potentially life-threatening opportunistic infection most often affects immunodeficient children, particularly those who are infected with HIV and have CD4 counts of less than 100 cells/mm³. The clinical onset is variable but often abrupt, with tachypnea, cough, and cyanosis. A marked decrease in the arterial oxygen saturation is seen, with a normal carbon dioxide level.

Imaging: The characteristic radiographic findings of P. jiroveci pneumonia are symmetric bilateral ground-glass opacities (Fig. 54-36). Such opacities may be diffuse but tend to involve predominately the perihilar regions or middle and lower lung zones.^132,133 Disease progression may result in more confluent, mainly perihilar or diffuse, bilateral airspace consolidation. The underlying pathophysiologic process is alveolar filling by a foamy exudate consisting of surfactant, fibrin, and cellular debris.^134–137 Associated interstitial edema or cellular infiltration may present on CT as septal thickening, intralobular thickening, or both.¹³⁸ The combination of such interstitial thickening and ground-glass opacities may produce a CT pattern known as “crazy paving”.¹³⁹ Terminally, massive consolidation may occur, often complicated by pneumothorax and pneumomediastinum.¹⁴⁰ Pleural effusions are rare.¹⁴¹

In 10% to 30% of patient with AIDS who received prophylaxis with aerosolized pentamidine and trimethoprim-sulfamethoxazole, a cystic form of the disease may evolve, characterized by either unilateral or bilateral upper lobe predominant thin-walled cysts.¹³⁸ Such pulmonary cysts are associated with pneumothoraces.¹⁴² In recent years, in spite of the advances in the prevention and treatment of P. jiroveci infection, several atypical presentations have emerged, including multiple pulmonary nodules, mass lesions, pleural effusion, and lymph node enlargement.^143–146

Treatment and Follow-up: Although imaging findings are not specific for P. jiroveci infection, the presence of bilateral ground-glass opacities in immunocompromised children should lead to this diagnosis.¹⁴⁷ Tracheal washings or lung biopsy, when performed, may show the organisms on microscopic examination after silver methenamine staining.

Etiology: Pulmonary candidiasis is almost always encountered in immunocompromised children, those with indwelling catheters, those who are undergoing prolonged antibiotic therapy, or those who are on steroids. Candida albicans is the responsible organism in the majority of candidal infections.¹⁴⁸ The organism regularly colonizes the upper respiratory tract and then spreads to the lungs. Pulmonary candidiasis may be either a primary infection (limited to the lungs) or a secondary infection (caused by hematogenous dissemination from other sites of infection).

Imaging: Although radiographs are often normal in the earliest stages of infection, nonspecific features of bronchopneumonia and lung nodules may be noted (e-Fig. 54-37).^148,149 Those nodules may cavitate, and unilateral or bilateral lobar or segmental opacities may also be seen.

Treatment and Follow-up: Children who are severely ill with pulmonary candidiasis receive antifungal therapy with triazole compounds and echinocandins, which are known for their excellent lung penetration.

Etiology: The lung fluke Paragonimus westermani is endemic in parts of Southeast Asia, South America, and Western Africa. In the United States, pulmonary paragonimiasis has affected refugee Indochinese children and Latin-American immigrants.151,152 Children are usually infected after ingestion of undercooked crustaceans, including crabs or crayfish, or by drinking contaminated water. In Southeast Asia, infestation of the lungs by P. westermani is said to be a common cause of pediatric lung necrosis and calcification, but it is difficult to differentiate from TB and fungal diseases on the basis of radiographic criteria alone (e-Fig. 54-38). Affected children usually present with fever, pleuritic chest pain, and respiratory symptoms such as chronic cough or hemoptysis. The diagnosis depends on a combination of findings, including history, peripheral blood eosinophilia, identification of ova in the stool or the sputum, and a positive ELISA (enzyme-linked immunosorbent assay) test result.

Imaging: Imaging findings depend on the stage of the disease. The early stage is characterized by (1) linear opacities, which are 2 to 4 mm thick and 3 to 7 cm long, extending inward from the pleura representing the migration of juvenile worms; (2) focal airspace consolidation, representing exudative or hemorrhagic pneumonia caused by the migrating worm; (3) pneumothorax; or (4) hydropneumothorax. Features of the late stage of infection include nodules, thin-walled crescent-shaped worm cysts (the “signet ring” sign), dense masslike consolidation, or bronchiectasis. As the flukes move from the abdomen to the chest, they penetrate the diaphragm and pleural layers, and thus pleural effusions and thickening are commonly noted.

Treatment and Follow-up: Pulmonary paragonimiasis is treated with antiparasitics such as praziquatel and bithionol.

Etiology: Echinococcosis or hydatid disease in humans is caused by infestation with Echinococcus granulosus (dog tapeworm). Humans are infected by direct contact with definite hosts (e.g., dogs) or by ingestion of eggs present in infected water, food, or soil. The eggs of E. granulosus hatch into larvae in the duodenum and are typically trapped within the liver (~75%) or lungs (~5% to 15%). They pass through the portal system in the liver or pulmonary alveolar capillaries, respectively. These larvae eventually develop into round or oval-shaped cysts within the liver or lungs (e-Fig. 54-39). Although most children with pulmonary involvement by hydatid disease are asymptomatic, they may present with fever, shortness of breath, cough, chest pain, which is usually a sign of cyst rupture. Diagnosis of hydatid disease depends on the combination of imaging and serology.

Imaging: The radiologic findings are characterized by single or multiple (~25%), round or oval-shaped, cystic nodules or masses (1-20 cm in diameter) with well-defined walls, surrounded by normal lung parenchyma (see e-Fig. 54-39). Other findings include an air-crescent sign, when a cyst communicates with a bronchus, or the water-lily sign (Fig. 54-40), when a cyst membrane floats in residual fluid after cyst rupture.^140,141 Pericystic emphysema may be a sign of impending rupture. After rupture of the cysts, cavitation or abscess formation and bronchiectasis may occur.

Treatment and Follow-up: Traditionally, surgical removal of the pulmonary cysts, often with supplemental medication such as benzimidazole, has been performed. Despite the risk of anaphylactic reactions following cyst aspiration, careful image-guided percutaneous techniques appear to be sufficiently safe.¹⁵³