Chapter 35. Recurrent Pneumonia

A child presenting with recurrent respiratory infections or radiographic abnormalities poses a common diagnostic problem for general pediatricians and pulmonary specialists alike. Pneumonia can be described both in clinical and radiographic terms. The World Health Organization defines pneumonia clinically as cough or dyspnea in association with labored breathing or tachypnea, and radiographically as an opacity occupying at least part of a single lobe and up to the entire lung.1,2 The incidence of pneumonia in developed countries is approximately 3–3.6 children per 100, whereas in developing countries, it can reach as high as 40 per 100 children.3 Recurrent pneumonia has been defined as two episodes in 1 year or 3 in a lifetime, with radiographic clearing between episodes.4 The incidence of recurrent pneumonia among large populations of children is unknown.

Several series have described both the frequency of recurrent pneumonia, as well as the leading causes for such, in various smaller populations of children. These studies demonstrate that the majority of children with recurrent pneumonia have an identifiable cause for their recurrent symptoms. The most common cause, however, varies depending on the characteristics of the population of children studied, whether inpatient or outpatient, referred to a subspecialty or general pediatric service, or from developed or developing countries. In a 10-year review of hospital records at a tertiary care children's hospital, 8% of 2952 children with pneumonia had a recurrent episode.5 Of those 238 children, 92% had an “underlying illness.” The leading diagnosis was oropharyngeal incoordination with aspiration, occurring in 48%, followed by immune disorders. Lodha et al.6 reviewed all children presenting to a pediatric pulmonary clinic in New Delhi in a 4-year period. Children were included in the analysis, if they met clinical criteria and had radiographic confirmation of pneumonia. Additionally, children with cystic fibrosis and congenital heart disease were excluded. Seventy children of 2264 (3.1%) in a 5-year period met these standards. An underlying illness was diagnosed in 84% of children; the most common diagnosis was recurrent aspiration, in 24.2% of children, followed by immune deficiency and asthma. In contrast, Ciftci et al.7 reviewed all children admitted to the pediatric infectious disease service of a tertiary care hospital in Turkey. Children without radiographic diagnostic confirmation were excluded from analysis. Nine percent of 288 patients met the criteria. Underlying disease was identified in 85% of patients, with asthma occurring in 32%, and therefore the most common diagnosis. Swallowing dysfunction was present in only 3%. Children with cystic fibrosis and congenital heart disease were included in this analysis.

Eigen et al.8 found similar results in a population of children referred to a tertiary care pediatric hospital for evaluation of persistent or recurrent pneumonia. Children were divided into two groups—those with apparent causes for persistent or recurrent radiographic densities, and those without. Approximately 50% of those in the group with predisposing causes had either gastroesophageal reflux or oropharyngeal incoordination. Of the group with no apparent condition, nearly half had a family history of atopy, 20% were wheezing at the time of evaluation, and 92% of those old enough (>5 years) to be evaluated by spirometry, demonstrated bronchial hyperresponsiveness. Children in Haiti who were diagnosed with recurrent pneumonia based on World Health Organization clinical criteria were compared with children who had never been diagnosed with pneumonia.9 Seventy-nine percent of 103 children with recurrent pneumonia had a history of wheezing, and 36% had wheezing with exercise, both higher percentages than in those children without a history of pneumonia.

Infection of lung parenchyma can occur whenever protective mechanisms are overcome or circumvented. Particles larger than 10 μm are filtered out in the nose, and particles between 2 and 5 μm typically impact on the airway mucosa where they can be removed by the mucus lining layer and mucociliary escalator. Laryngeal structures, including the epiglottis and vocal cords, protect the airway from aspiration of oropharyngeal material during deglutition and from gastric contents if gastroesophageal reflux is present. Cough is a critical mechanism to clear the airways of particles and infecting organisms, and acts as a backup mechanism if the mucociliary escalator or laryngeal defenses are ineffective or overcome. Both the innate and adaptive immune systems operate in the lung to help clear infecting organisms. The former includes a host of molecules like complement, adhesion proteins, collectins, and toll-like receptors. Adaptive immunity includes mast cells, dendritic cells, and macrophages, as well as circulating immunoglobulins. The principal protective immunoglobulin of the upper airway is IgA, while IgG is chiefly responsible for protection of the lower airways and alveoli.

While any of these mechanisms can be overcome by chance, leading to an episode of pneumonia, it is the persistence of an abnormality of some aspect of the lung's defense system that predisposes to recurrent episodes of pneumonia. Thus, impaired cough, structural abnormalities that preclude adequate airway clearance, ineffective physical defense mechanisms to prevent soiling of the lung, an abnormality of mucus or of ciliary function, or a breakdown of host immune function are all possible causes for a child to experience recurrent pneumonia.

The clinical presentation of recurrent pneumonia will depend principally on the underlying cause (Table 35–1). Children who have an anatomic defect that predisposes to pneumonia recurrences in a single region will often have no other sign of systemic disease. If bronchiectasis occurs in the region, however, there may be a history of weight loss, or of poor weight gain and of digital clubbing, likely a reflection of a chronic suppurative condition in the chest. Those children who develop recurrent pneumonias in different regions of the lung usually present with other findings beyond fever, cough, and chest crackles. Children with asthma as a cause for recurrent pneumonia typically will be diagnosed during an acute exacerbation of asthma symptoms. Approximately 85% of children with cystic fibrosis also have pancreatic insufficiency, so that symptoms of intestinal malabsorption and growth failure will be present. Infants and children with swallowing dysfunction often have a history of coughing or choking during feedings. While gastroesophageal reflux may be silent, more often there is a history of arching during meals (if esophagitis is present), rumination, frequent effortless regurgitation (“wet burps”) or frank emesis. These are frequently accompanied by contemporaneous alterations in the respiratory examination, like tachypnea, cough, or coarse breath sounds. Children with systemic immune deficiencies or primary ciliary dyskinesia will have prominent upper respiratory findings, like recurrent otitis, pansinusitis, and chronic purulent rhinitis. Some immunodeficiency states, like chronic granulomatous disease (CGD) or hyper IgE syndrome also predispose children to recurrent skin infections.

The first important determinant in creating a differential diagnosis is establishing if the disease process has involved the same location or different areas of the lung (Table 35–2). In actual practice, this division depends on both a cogent historian and the availability of radiographic data.

Same Location

Pathology affecting a single region can be related to obstruction of the airway lumen that subtends the area by intraluminal obstruction or compression, intrinsic narrowing of the airway, or an abnormality of the involved parenchyma. Causes of intraluminal obstruction include such entities as foreign body, tumor, or mucous plug. Compression of the airway is seen with lymphadenopathy from various causes, including infection—such as tuberculosis, histoplasmosis, and other mycotic infections—and from noninfectious causes, including sarcoidosis and neoplasms. Additionally, external compression can arise from an abnormality of the vasculature, such as a vascular ring, or from mediastinal tumors or duplication cysts.

Structural airway abnormalities that cause retention of secretions can result in chronic or recurrent infection.10 These include anomalies of airway configuration, such as a tracheal bronchus, which is a right upper lobe bronchus that emanates from the trachea, rather than from the right main bronchus. When its orifice is smaller than normal or the airway takes off from the trachea at an acute angle, the airway is prone to obstruction from secretions. Similarly, a “bridging bronchus,” a right lower lobe bronchus that arises from the left bronchial tree, can impair proper drainage. Localized bronchial stricture or stenosis occurs most commonly in a main or middle lobe bronchus,11 but these lesions can also occur in the distal trachea; especially when acquired as a result of airway intubation and suctioning.12–14 Bronchial atresia may be asymptomatic, or can result in lobar degeneration distal to the obstruction, leaving a mucus-filled or fluid-filled cystic structure in its place, which can then become infected. Bronchomalacia, or excessive collapsibility of the airway wall, predisposes to retained secretions. Localized bronchiectasis may be congenital, which is rare, or be a result of chronic localized infection or a prior viral illness.15

Right middle lobe syndrome is an entity described in both the pediatric and adult literature in which a recurrent radiographic density associated with respiratory symptoms occurs in the right middle lobe region (Figure 35–1). It requires special mention, because of the unique nature of the anatomy of the right middle lobe. The normal anatomy of the right middle lobe—the airway's acute angular take off from the bronchus intermedius, narrower caliber, and longer distance without branching, as well as the lack of collateral ventilation to the lobe itself—predisposes to difficulties with airway clearance and retained secretions. Asthma is the most common underlying disorder associated with the right middle lobe syndrome. Bronchoscopic findings in 52 of 55 children with middle lobe syndrome included airway mucosal edema, retained secretions, and mucus plugging, rather than complete obstruction. Additionally, more than half of these patients had elevated eosinophils in lavage fluid.16,17

Congenital lung malformations become infected as a result of either abnormalities in the airways leading to them, or compromised blood flow to them. Bronchogenic cysts, which result from aberrant budding of the tracheobronchial tree during development, are often located centrally and on the right. These unilocular structures do not communicate with the airway, although they may carry their own blood supply. They can become infected, or they may cause symptoms by compressing adjacent airways and impeding airway clearance. Bronchogenic cysts will appear radiodense initially, but become lucent when infected.18 Congenital cystic adenomatoid malformations (CCAM) are lesions in which varying degrees of cystic and glandular structures replace normal alveolar tissue. A CCAM usually involves a single lobe, unlike bronchogenic cysts, CCAMs communicate with the tracheobronchial tree. On radiographs, CCAMs appear as uni- or multiloculated lucent or dense structures. Pulmonary sequestrations are masses of lung parenchyma usually without connection to the tracheobronchial tree, but with a defined systemic blood supply, usually arising from the aorta. Sequestrations can be intralobar (invested in the pleura of normal lung) or, less commonly, extralobar (covered with their own pleura). Intralobar sequestrations are found most commonly in the left lower lobe and most often present as recurrent pneumonia. Radiographic appearance is initially radiodense, but, with infection, the degree of lucency can increase.

Different Locations

Recurrent pneumonia involving different locations often is associated with a systemic disease process. Aspiration has been described in several case studies as the most common cause of recurrent pneumonia.5,6 Recurrent pneumonia from aspiration itself can also be associated with several other conditions. Impaired swallowing with inadequate airway protection can result from a variety of neuromuscular disorders, including cranial nerve injury, cerebral palsy, and muscular dystrophy. Anatomic abnormalities of the larynx including vocal cord paralysis or laryngeal cleft compromise airway protection. Esophageal obstruction, from foreign body, foregut malformation, or vascular ring may impair the normal swallow and worsen reflux of gastric contents. Similarly, esophageal dysmotility, from achalasia or tracheoesophageal fistula, also predisposes to aspiration19 (Figure 35–2).

Asthma is one of the most common causes of recurrent pneumonia. Undertreated asthma is associated with airway inflammation, increased mucus production, and luminal narrowing from airway wall edema. Whether radiographic densities seen during acute exacerbations represent true areas of infection or atelectasis is often uncertain. Recent data using sensitive detection techniques, however, suggest that acute viral infections account for as much as 85% of asthma exacerbations in school-aged children.20

Malfunction or deficiency in any component of the immune system, adaptive or innate, often leads to recurrent pulmonary infections. It is extremely unlikely, however, for a child to have recurrent pneumonia from an immunodeficiency without also having a history of recurrent otitis or sinusitis, and chronic purulent rhinitis. A clear way to classify these defects is into disorders of phagocyte function, B cell function, and T cell function. The most common example of phagocyte dysfunction in children with recurrent pulmonary disease is chronic granulomatous disease (CGD). Children with CGD, with an incidence of 1 in 20,000, experience severe pneumonia and abscesses. Most often, infections are caused by catalase positive organisms like Staphylococcus aureus, Aspergillus spp., Burkholderia cepacia, Nocardia spp., and Serratia spp. These infections occur as a result of a loss of NADPH oxidative function. Hyper IgE, or Job, syndrome is associated with severe pneumonia, often resulting in pneumatocele formation, eczema, and coarse facial features. The immune defect in hyper IgE syndrome is unclear, but has been hypothesized to relate to neutrophil dysfunction.21

Defects in B cells result in problems with formation of antibodies, which are essential for opsonization and clearance of encapsulated organisms, such as Streptococcus pneumoniae and Haemophilus influenzae. These defects often present in late infancy, after maternal IgG is cleared. X-linked, or Bruton's, agammaglobulinemia, presents with recurrent pneumonias as well as Pneumocystis carinii (now P. jirovecii) infection. Common variable immune deficiency (CVID), in which there are varying low levels of immune globulins, especially gamma globulin, does not present with opportunistic pathogens, but with recurrent bacterial infections of the sinuses or lungs. If not diagnosed in childhood, individuals with CVID often develop bronchiectasis as adults.22 IgG subclass deficiencies also can present with recurrent pneumonia. Most is known about IgG2 deficiency, which often presents as asthma. The most common immune globulin defect is IgA deficiency, with an incidence of 1/400–3000. IgA deficiency often coexists with an IgG subclass deficiency. A recent study, however, found that although 50% of a population of IgA-deficient patients presenting to an immunology clinic for evaluation had recurrent respiratory infections, they were not more likely to have an associated IgG2 subclass deficiency or poor responses to the pneumococcal vaccine.23

T cells have populations of antigen-presenting or helper cells as well as killer cells. T cells are responsible for the orchestration of the adaptive immune system, as well as direct elimination of viruses and fungi. Severe combined immune deficiency, in which both T cell and B cell function is severely reduced or absent, presents early in infancy. 67% of patients with severe combined immune deficiency have pulmonary disease at diagnosis and are susceptible throughout life to opportunistic pathogens. Other T cell deficiencies can present more subtly. Children with DiGeorge syndrome, associated with 22q11 microdeletion, absent 3rd and 4th pharyngeal pouches, thymic aplasia to hypoplasia, and hypoparathyroidism have a range of immune defects, most commonly pneumonia caused by Gram-negative bacteria and severe respiratory syncytial virus infection. Those with absence of the thymus have more severe defects and are at risk for pneumocystis infections. Several conditions present with subtle and combined immune problems, relating to interaction between T and B lymphocytes. Wiskott Aldrich syndrome is an X-linked recessive condition with thrombocytopenia, eczema, and recurrent bacterial infection. Immune defects include lymphopenia and a decreased response to polysaccharide antigens.24 Ataxia-telangiectasia is a progressive neurologic disorder associated with varying degrees of immune deficiency and recurrent pulmonary involvement.25

A local defense mechanism that is critical for clearing the airways of inhaled debris and infecting organisms is the mucociliary escalator. Dysfunction of the mucociliary clearance system occurs in both cystic fibrosis and primary ciliary dyskinesia. In cystic fibrosis, the airway surface liquid is depleted, resulting in increased mucous viscosity and an inability of the cilia to clear airway secretions effectively. Because of the increased mucus viscosity, cough becomes ineffective at clearing secretions. In contrast, primary ciliary dyskinesia affects only the beating action of the cilia, and the mucus itself is normal; cough is effective in this case. In both conditions, however, mucus stasis results in recurrent infections and ultimately leads to bronchiectasis.

Diffuse processes such as hypersensitivity pneumonitis, allergic bronchopulmonary aspergillosis, or eosinophilic pneumonia represent abnormal immunological responses. While these entities do not cause pneumonia per se, recurrent radiographic densities are prominent features in each. Similarly, children with recurrent pulmonary hemorrhage or sickle cell disease can develop diffuse densities and respiratory symptoms with varying degrees of clearing. It is occasionally difficult to distinguish pneumonia in children with sickle cell disease from acute infarction.

History and Physical Examination

Making the diagnosis of recurrent pneumonia begins with history-taking and physical examination. Symptoms that begin in early infancy point to congenital structural lesions, serious immune deficiency, or other inherited diseases like cystic fibrosis or primary ciliary dyskinesia. Another important historical point is the persistence—or absence—of such symptoms when the patient is well. Most children with immunodeficiency will have persistent upper respiratory evidence of infection, for example, purulent rhinitis, recurrent sinusitis, or otitis, especially when they are not receiving antibiotics. Thus, a history of purulent nasal discharge that recurs whenever the child is taken off antibiotics should prompt a screening of immune function. A recalled episode of choking demands evaluation for foreign body, although one-third of children with a foreign body aspiration will have no such history. Respiratory symptoms that worsen during or shortly after feedings point to possible swallowing dysfunction with or without gastroesophageal reflux. Similarly, when symptoms occur during or soon after an acute viral upper respiratory illness, asthma should be considered as the likely cause of lower respiratory findings. It is helpful to get a history of wheezing during acute episodes, but this is a highly nonspecific finding and other respiratory sounds are often mislabeled by parents as wheezing. In contrast, a history of responsiveness to bronchodilators is once again supportive of a diagnosis of asthma.

Symptoms outside of the respiratory system can also yield important clues to the etiology of recurrent pneumonia. Intestinal malabsorption occurs in 85–90% of children with cystic fibrosis. Recurrent skin infections occur in several immunodeficiency states, and a history of severe eczema can reflect atopy and possible asthma, or immunodeficiency.

Elements in the social history, such as exposure to cigarette smoke and pollutants, or daycare and its exposure to multiple viruses, can point to an etiology such as asthma. Travel history assesses exposure to infectious agents such as tuberculosis, histoplasmosis, and parasites. A family history of early or unexplained death points toward immune deficiency or other systemic diseases like cystic fibrosis.

As with the history, the physical examination should be directed to both sinopulmonary and extrapulmonary findings. Dysmorphic features can be associated with a structural anomaly, or point to an immune deficiency, like DiGeorge syndrome. Growth parameters should be assessed, since failure to thrive suggests a pervasive systemic disease.

The upper respiratory tract yields important clues as to the cause of recurrent chest infections. Dennie's lines, shiners, a transverse crease over the nasal bridge, and scaling of the skin suggest atopy. Otitis media, purulent rhinitis and sinusitis prompt further evaluation for immune deficiency or ciliary dyskinesia. The presence of nasal polyps in children is overwhelmingly associated with either cystic fibrosis or severe allergic rhinitis. Their presence should always be cause to obtain a sweat test. Periodontal disease and candidiasis can point to immune deficiency. Digital clubbing often reflects a pyogenic process in the chest, like bronchiectasis or pulmonary abscess, although it is also present in patients with cyanotic congenital heart disease, inflammatory bowel and liver disease, and bacterial endocarditis. These causes can usually be easily distinguished.

Physical assessment of the respiratory system can point to particular etiologies of recurrent pneumonia, and also will reflect the severity of the underlying condition. Tachypnea, dyspnea with retractions, use of accessory muscles, and oxyhemoglobin desaturation all point to significant and probably widespread disease. Auscultation should include an assessment of air movement, comparison of the right and left sides, and individual regions. Wheezing that is comprised by the same set of sounds transmitted throughout the chest (homophonous wheezing) signifies a central airway obstruction like a retained foreign body, airway compression, or tracheobronchomalacia. Wheezes that contain different sets of sounds regionally reflect peripheral airway obstructions of different degrees, like those that exist in asthma.

Cardiac examination may reveal the presence of situs inversus, associated with 50% of cases of ciliary dyskinesia (Figure 35–3), presence of a cardiac lesion, or heart failure.

Diagnostic Testing

Testing should be guided by the individual situation (Table 35–3 and Figure 35–4). A chest film, both posterior–anterior and lateral, should be a part of the evaluation of every patient with recurrent pneumonia. All prior examinations should be reviewed as well. Ideally, a film should also be taken when the patient is well to differentiate whether the problem is recurrent or chronic. If the patient is acutely ill, adequacy of gas exchange should be established with examination and arterial blood gas analysis. Sputum culture and Gram stain in those who can expectorate aid in establishing the microbiology of an infection—and may refine further the differential diagnosis.

In those with recurrent or persistent focal abnormalities, evaluation is geared to defining abnormalities of the airway—whether internal or external. Bronchoscopy (airway endoscopy) provides direct visualization of airway anatomy and allows assessment for presence of foreign body and extraluminal compression, as well as performance of lavage for culture. If a retained foreign body is highly suspected, then the study of choice is rigid (open tube) bronchoscopy under general anesthesia. Otherwise, flexible bronchoscopy, especially under conscious sedation, offers the advantages of more distal airway inspection and an opportunity to see dynamic events, like airway collapse on exhalation. Bronchoalveolar lavage should also be considered in children with recurrent pneumonia in different locations, if they are unable to produce sputum and identification of the infecting organism is desired.

Chest computed tomography (CT) allows for localization of a possible extraluminal airway compression—such as by a lymph node—as well as refinement of the anatomic location of radiographic densities. The CT scan also provides excellent visualization of the involved parenchyma and can be diagnostic for bronchiectasis as well as several congenital lesions. There has been recent interest in multidetector CT scan with virtual tracheobronchoscopy as a less invasive alternative to conventional airway endoscopy.26

There are several choices for evaluating the great vessels and the possibility of a vascular ring (Figure 35–5). The choice of which to use will depend on local availability and expertise. A barium esophagram reflects the type of vascular ring from the pattern of compression on the esophagus. More recently, CT angiography and magnetic resonance imaging have been refined to define vascular anomalies with a high degree of accuracy.27

Adjunctive testing is aimed at detecting specific diseases. Purified protein derivative should be placed when the history or radiographic findings are suspicious for tuberculosis, and evaluation for fungal infections such as aspergillosis and coccidiomycosis should also be performed. The sweat test, quantitative immunoglobulins with subclasses, complete blood count with differential, antitetanus and diptheria titers, and ciliary biopsy should be performed if the diagnosis is likely to be cystic fibrosis, an immunodeficiency, or primary ciliary dyskinesia. As untreated asthma has been shown to be one of the most common causes for recurrent pneumonia, spirometry, to assess for evidence of airways obstruction and response to bronchodilator, should be performed. In those children who cannot perform spirometry, an alternative is a therapeutic trial of inhaled corticosteroids and bronchodilators for a defined time period.

In those with neurologic dysfunction, evaluation of swallowing function, including a fluoroscopic video swallowing study and scintigraphy to evaluate for both gastroesophageal reflux and abnormal swallow, should be performed.28 A functional endoscopic swallow study can provide increased information regarding the patient's actual swallow function.

Treatment depends on identifying the underlying cause of recurrent symptoms and whether or not the child is acutely ill. Supplemental oxygen, antibiotics, and ventilatory support should be administered as appropriate. In a patient with recurrent pneumonia, broad-spectrum antibiotic therapy is typically warranted; options include ampicillin-sulbactam, cefotaxime, or piperacillin-tazobactam. Clindamycin or vancomycin should be added to provide coverage against methicillin-resistant S. aureus if the patient is severely ill at presentation or if the initial response to therapy is poor.

If there is a problem with retention of secretions, chest physiotherapy or other methods of airway clearance are indicated. When such measures fail and there is a concern for mucous plugs obstructing a central airway, bronchoscopy can be considered to help improve airway clearance. In addition to its role in diagnosis, bronchoscopy has been shown to be therapeutic in aiding resolution of the right middle lobe syndrome.16 Certain children with underlying diseases, like cystic fibrosis, primary ciliary dyskinesia, and immunodeficiencies, respond well to administration of chronic courses of antibiotics. Often, this is determined on an individual basis, but there are some conditions like X-linked agammaglobulinemia where a role for chronic antibiotic use has been established. In patients with CVID, regular administration of gamma globulin reduces the frequency of pulmonary infections29 (Figure 35–6).

Surgical treatment for recurrent pneumonia is indicated when congenital malformations of the lung are discovered, or if lesions compress an adjacent bronchus.30 Vascular rings that compress airways and possibly the esophagus should be divided. Abnormal connections between the airway and digestive tract, for example, H-type tracheoesophageal fistula or laryngotracheoesophageal cleft, must be repaired to halt recurrent soiling of the lung.

For children with recurrent pneumonia relegated to a single region, the outcome is usually excellent. Often, excision of the offending lesion results in complete resolution of the problem.30 Less commonly, lobectomy is considered when the affected area acts as a nidus for recurrent infections to the remainder of the lung. The course and prognosis for children whose recurrent pneumonia varies regionally usually follows that of the underlying disease and the tools available for treatment. For instance, the prognosis of a child with recurrent pneumonia related to immunoglobulin deficiency can be excellent with replacement therapy and judicious use of antibiotics. For the most common situation that physicians in developed countries will encounter—asthma—the prognosis is good. With adequate therapy with inhaled corticosteroids, asthma (usually) can be effectively managed. Management of recurrent aspiration of oropharyngeal secretions can be somewhat more challenging. With appropriate augmentation of airway clearance therapies, patients with primary ciliary dyskinesia can be expected to have a normal life span. The outcome for those with cystic fibrosis is somewhat more guarded.

• Single or varied regional involvement provides a useful way to guide diagnostic evaluation.
• Always consider undertreated asthma in a child with either uni- or multifocal disease that occurs following common upper respiratory infections.
• The underlying disease predisposing the patient to recurrent pneumonia is often already known.
• However, recurrent pneumonia, especially in children who have growth disturbance, may be the first sign of an immune deficiency.
• If untreated—and sometimes even if treated properly—recurrent pneumonia predisposes to bronchiectasis later in life.