Pulmonary Infection

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. 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. 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, and bronchiectasis, best seen on computed tomography (CT). Swyer–James–MacLeod syndrome, the result of bronchiolitis obliterans in the growing lung, 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.

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 ).

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

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 after 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. Adenopathy is more common than in other viral pneumonias. Bronchiectasis or bronchiolitis obliterans may be a permanent sequel (see e-Fig. 54.2 ).

In children infected with CMV, a progressive interstitial pneumonitis is seen ( e-Fig. 54.5 ). CT findings are nonspecific, with ground-glass opacities and consolidations in 80% of the cases. Gallium-67 scintigraphy may show abnormal uptake in the lungs of patients who have a normal chest CT.

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.

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. With a few exceptions, the use of extracorporeal membrane oxygenation to treat severe respiratory failure from ARDS, which frequently complicates severe infections, has not led to better outcomes than those of optimal less invasive supportive care. Certain high-risk infants may qualify for prophylactic injection of monoclonal antibodies against the F-glycoprotein of RSV. Because 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.

Etiology.

Streptococcus pneumoniae is the most common cause of bacterial pneumonia in children less than 5 years of age. It is a gram-positive diplococcus that infects healthy patients but also commonly attacks those with underlying illness, including the hospitalized and immunocompromised, and children with sickle cell anemia. A strong association with a preceding viral infection, in particular influenza, is seen. The virally activated respiratory epithelium has an increased expression of receptors for pneumococcal attachment. In the usual case of an infected but otherwise healthy child, the onset is acute with fever, headache, and abdominal or chest pain with respiratory symptoms and signs. 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 . After 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%.

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. Large pleural effusion, empyema, and lung necrosis 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 1 year of age (70%). 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. 54.9 ). 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. 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.

The more invasive and virulent strains of S. aureus, which carry the genetic marker Penton-Valentin leucocydin (PVL), are responsible for the most serious primary or metastatic infections of the lungs that are acquired in community settings.

Imaging.

In contrast to pneumococcal pneumonia, staphylococcal pneumonia is a lobular or bronchopneumonia, which begins in the airways rather than in the alveoli ( e-Fig. 54.10 ). 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. Ten percent of children with staphylococcal pneumonia have a pneumothorax, which may result from the rupture of a pneumatocele. Pleural effusion and empyema are also very frequent, occurring in more than 90% of children ( Fig. 54.11 ).

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

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 called “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. 54.12 ). However, nonspecific findings such as hyperaeration, atelectasis, segmental consolidations, and hilar lymphadenopathy are seen more commonly. 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.