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S E C T I O N V   Pediatric Critical Care: Pulmonary

• BOX 52.1 Etiology of Pediatric Interstitial Lung

Disease
Infectious
•
•
•
•
•
•
•

Bacteria
Virus
Mycoplasma
Chlamydia
Rickettsia
Protozoa
Fungus

Noninfectious
•
•
•
•
•
•

•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•

Acute lung injury
Chemical agents
Physical agents
Radiation
Drugs
Congenital lymphangiectasia
Metabolic disorders

Bronchopulmonary dysplasia
Hypersensitivity pneumonitis
Cardiovascular causes
Collagen/vascular disorders
Mixed connective tissue disorders
Idiopathic pulmonary fibrosis
Pulmonary hemorrhage syndromes
Pulmonary hemosiderosis
Pulmonary venoocclusive disease
Desquamative interstitial pneumonia
Lymphocytic infiltrative disorders
Lymphocytic interstitial pneumonitis
Familial erythrophagocytic lymphohistiocytosis
Angioimmunoblastic lymphadenopathy
Sarcoidosis
Inherited diseases
Malignancy
Leukemia
Hodgkin disease
Non-Hodgkin lymphoma
Histiocytosis X

lung volumes and pulmonary compliance occurs as the disease
progresses, leading to pulmonary fibrosis.1 Expiratory flow rates
are usually preserved in persons with pneumonitis involving the
lung parenchyma, and major obstructive defects, although reported, are rare. Diffusion capacity, one of the earliest and most
sensitive tests of parenchymal inflammation, is diminished in
persons with interstitial lung disease (ILD). A reduction in diffusion capacity is not specific and may be found with other parenchymal disorders. Early in the course of parenchymal disease,
resting arterial oxygen tension may be normal, but there is often
mild alveolar hyperventilation with reduction in alveolar carbon

dioxide tension and widening of the alveolar-arterial oxygen gradients (Pao2 – Pao2). With exercise, hypoxemia and an increased
Pao2 – Pao2 become exaggerated because of ventilation/perfusion
(V/Q) imbalance. V/Q mismatch is attributed to regional alterations of flow, altered parenchymal compliance, and increased obstruction to pulmonary airflow. Progressive alveolitis and subsequent derangement of gas exchange lead to deterioration of
ventilatory efficiency and markedly increased work of breathing.
Adequate oxygenation may become impossible even with the
use of high-flow supplemental oxygen. Resting hypercapnia,

pulmonary hypertension, and eventual right ventricular dysfunction with heart failure are common sequelae.1–4

Diagnosis
Diagnosing parenchymal lung disease in the pediatric patient may
be quite challenging because of extreme variability in the presentation of disease. Clinical evaluation of the child should include a
search for symptoms and signs associated with pulmonary disease,
such as difficulty with feeding, exercise intolerance, chest pain,
cough, tachypnea, dyspnea, cyanosis, orthopnea, clubbing of the
nail beds, weight loss, and lethargy. In the child with diffuse
alveolar disease, auscultative findings may be normal unless significant consolidation or small airway involvement is present. Fine
crackles that may be heard throughout the chest late in inspiration
are a characteristic finding of small airway disease. These rales are
produced by the opening of occluded small peripheral airways.

Laboratory Diagnosis
The chest radiograph is critical in the diagnosis and management
of pulmonary parenchymal disease. In children with ILD the classic radiographic features that are present in adults may be absent.
Computed tomography scanning,5–7 gallium lung scanning, and
bronchoalveolar lavage (BAL)8–10 are useful techniques in the
diagnosis and management of diseases involving the lung parenchyma. Pulmonary function testing is important and usually can
be performed reliably in children who are older than 4 years.1,11

Bacterial Pneumonitis

Bacterial infections of the lower respiratory tract continue to account for a significant number of hospital admissions. The frequency of bacteria as etiologic agents of lower respiratory tract
infection varies from 10% to 50% depending on the study population and methods of evaluation used.12,13 In a large study of
pediatric patients with lower respiratory tract infections, an etiologic agent was identified in nearly 50% of the patients. Bacteria
accounted for 10% to 15% of the causative agents identified.
Factors predisposing to bacterial pneumonia include having
numerous siblings, smoke exposure, preterm delivery, living in an
urban environment, and poor socioeconomic status. Hospitalization also increases the risk of contracting bacterial pneumonia
because of the clustering of ill patients in confined areas, administration of immunosuppressive therapy, and various medical and
surgical interventions that enhance the opportunity for colonization and infection. Additional factors that increase susceptibility
to bacterial pneumonia include the presence of an airway foreign
body,14 impaired immune response,15–19 congenital and anatomic
lung defects, abnormalities of the tracheobronchial tree, cystic
fibrosis,20 and congestive heart failure.

Definition
Bacterial pneumonia is an inflammatory process of the lungs that
may involve interstitial tissue and pleura in its evolution but
always progresses to alveolar consolidation.

Pathophysiology
Pneumonia occurs when pulmonary defense mechanisms are
disrupted and bacteria invade the respiratory system by aspiration


CHAPTER 52  Pneumonitis and Interstitial Disease

or hematogenous spread. In most instances pneumonia appears to
be a consequence of aspiration of a high inoculum of pathogenic
bacteria. Viruses are often responsible for enhancing the susceptibility of the respiratory tract to bacterial infection. Less frequently,
bacterial pneumonia may be the result of defects in host immunity because of young age, underlying immune dysfunction, or

immunosuppressive therapy. Pneumonia may also occur when
host defenses are mechanically disrupted because of tracheostomy
or endotracheal intubation. The presence of respiratory pathogens
in the terminal bronchioles and alveoli induces an outpouring of
edema fluid and large numbers of leukocytes into the alveoli.2,21
Macrophages subsequently remove cellular and bacterial debris.
The infectious process may extend further within the lung segment
or disseminate through infected bronchial fluid to other areas of
the lung. The pulmonary lymphatic system enables bacteria to
reach the bloodstream or visceral pleura.
With the consolidation of lung tissue, VC and lung compliance markedly decrease. This leads to intrapulmonary right-to-left
shunt and V/Q mismatch, resulting in hypoxia. Subsequently,
pulmonary hypertension may develop because of significant oxygen
desaturation and hypercapnia, often leading to cardiac overload.

Clinical Features
Signs and symptoms of bacterial pneumonia vary with the individual pathogen, age and immunologic condition of the patient,
and severity of the illness. Clinical manifestations, especially in
newborns and infants, may be absent. General or nonspecific
complaints include fever, chills, headache, irritability, and restlessness. Individual patients may have gastrointestinal complaints,
including nausea, vomiting, diarrhea, abdominal distention, or
pain. Specific pulmonary signs include nasal flaring, retractions,
tachypnea, dyspnea, and, occasionally, apnea.
Tachypnea is the most sensitive index of disease severity. The
sleeping respiratory rate is often a valuable guide to diagnosis. On
auscultation, diminished breath sounds are frequently noted. Fine
crackles that may be heard in children and older patients are commonly absent in infants. Because of the relatively small size of the
child’s thorax and thin chest wall, broad transmission of breath
sounds occurs, and the classic findings of consolidation are often
obscured. Pleural inflammation may be accompanied by chest

pain at the site of inflammation. This pleuritic pain may cause
“splinting,” which restricts chest wall movement during inspiration and reduces lung volume.
Extrapulmonary infections that may be present in some children include abscesses of the skin or soft tissue (Staphylococcus
aureus); conjunctivitis, sinusitis, otitis media, and meningitis
(Streptococcus pneumoniae or Haemophilus influenzae); and epiglottitis (H. influenzae).

Radiographic Features
Bacterial pneumonia is typically characterized by defined areas of
consolidation with either segmental or lobar involvement. Lobar
consolidation is the most characteristic, but multilobed disease is not
unusual. The findings of pleural effusion, pneumatocele, or abscess
are also strongly indicative of a bacterial infection. Staphylococcal
pneumonia is suggested by the rapid clinical and radiographic progression of disease, particularly in a young infant. Evidence of an
abscess or pneumatocele further suggests a diagnosis of staphylococcal or gram-negative pneumonia, such as Klebsiella. Group A streptococcal pneumonia may initially present with a diffuse interstitial

587

pattern before the development of consolidation. Except for Pseudomonas, which may have a diffuse nodular appearance in the lower
lobes, pneumonias caused by gram-negative organisms have no specific radiographic pattern. Anaerobic pulmonary infection is also
associated with lung abscesses and air-fluid levels.

Diagnosis
Bacterial pneumonia is suggested by fever, leukocytosis (.15,000
white blood cells), and increased band forms on the peripheral
blood smear. Examination of the sputum may be helpful in establishing the diagnosis of bacterial pneumonia; however, it is often
difficult to obtain a satisfactory sputum sample in pediatric patients unless transtracheal aspiration or bronchoscopy is used.
Transtracheal aspiration, although useful in adolescents and
adults, is associated with significant complications in infants and
young children. If a sputum sample is obtained (an adequate
specimen must have more than 25 polymorphonuclear cells and

fewer than 25 epithelial cells per high-power field), the Gram
stain should be examined for a predominant bacterial pathogen
and cultures should be performed with the appropriate antibiotic
susceptibility studies. Bacterial pneumonia is accompanied by
bacteremia in a significant number of cases; hence, blood cultures
should be obtained before initiation of antibiotic therapy. Circulating antigens in S. pneumoniae and H. influenzae may be detected in the blood with counterimmune electrophoresis (CIE),22
polymerase chain reaction (PCR),23–25 or latex agglutination.26,27
If a significant pleural effusion is present, a diagnostic thoracentesis should be performed for the purposes of Gram stain and
culture. Culturing pleural fluid has a relatively high yield in patients who have not received previous antibiotic therapy. If the
Gram stain of pleural fluid is negative, CIE or latex agglutination
should be performed because bacterial antigen may be detected in
the fluid even after the initiation of antibiotics.
BAL should be considered in the management of a severely ill
child in order to make a prompt diagnosis.9,10 Making a prompt
diagnosis is essential for the patient with progressive disease who
has responded poorly to initial therapy or for the child with underlying immunodeficiency for whom empiric antibiotic treatment may be hazardous. In such instances, if the BAL is nondiagnostic, then lung aspiration or biopsy should be considered.28
Material may be obtained through closed-needle biopsy, percutaneous needle aspiration, or an open-lung biopsy. Positive results
for such procedures in carefully selected cases identify an etiologic
agent in 30% to 75% of cases, with open-lung biopsy having the
highest yield.18,29

Specific Pathogens
Group B Streptococci
Group B streptococci can cause infection in people of any age;
however, these organisms are common pathogens in infants
younger than 3 months.30 Early-onset illness is often associated
with maternal fever at the time of delivery, prolonged rupture of
membranes, amnionitis, prematurity, and low birth weight.
Infected neonates usually manifest clinical symptoms within
the first 6 to 12 hours of life. Symptoms include fever, respiratory

distress, apnea, tachypnea, and hypoxemia. By 12 to 24 hours of
age, signs of cardiovascular collapse are often apparent. Frequently, the syndrome of pulmonary hypertension of the newborn is present, and pulmonary or intracranial hemorrhage may
become the terminal event.


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S E C T I O N V   Pediatric Critical Care: Pulmonary

Isolation of the organism establishes the diagnosis. Cultures
from blood and cerebrospinal fluids must be obtained in all instances of suspected group B streptococcal pneumonia. Rapid
diagnostic techniques have been helpful in providing early diagnoses. The radiographic findings in neonates with group B streptococcal pneumonia can be either a lobar (40%) or a diffuse reticulonodular pattern with bronchograms similar to findings of
respiratory distress syndrome.
Aggressive cardiovascular and ventilatory support is usually
required, particularly in the early stages of the disease. Antibiotic
therapy should include a combination of ampicillin or penicillin
and an aminoglycoside agent.
Although in the past the mortality rate of patients with group
B streptococcal pneumonia could be as high as 50% to 60%, recent studies suggest improvement with prompt initiation of therapy and even better outcomes with maternal prophylaxis.31 Some
infants experience a second episode of infection 1 to 2 weeks after
discontinuation of antibiotic therapy. Infants with group B streptococcal pneumonia and meningeal involvement (30%) may
demonstrate significant neurologic deficits (20%–50%).

Streptococcus Pneumoniae
S. pneumoniae is a gram-positive diplococcus with at least 84 sera
types; however, 80% of the serious infections are caused by only
12 sera types. Streptococci are a major cause of pneumonia in the
United States, usually affecting infants younger than 2 years, with
a peak age between 3 and 5 months. Patients with asplenia, functional hyposplenia, or malignancy or those receiving immunosuppressive drugs are at special risk of the development of invasive
disease.32

The radiographic finding in infants is often a patchy bronchopneumonia. Lobar consolidation is not uncommon. Penicillin is
the drug of choice in the treatment of persons with streptococcal
pneumonia. However, organisms relatively resistant to penicillin
occur in 3% to 40% of culture-positive patients recorded in studies from different parts of the United States.33 In such instances
pneumonias have been effectively treated with vancomycin or
high-dose b-lactam cephalosporin agents, such as cefuroxime,
ceftriaxone, or cefotaxime. Disease resulting from penicillin-resistant
pneumococci should be considered in patients who received
therapy with b-lactam antibiotics.33–35
The pneumococcal 13-valent conjugate vaccine is recommended for all children aged 5 years and younger. It is also recommended for certain children aged 60 to 71 months with chronic
medical conditions, immunosuppressive conditions, functional or
anatomic asplenia, cerebrospinal fluid leaks, or cochlear implants.
The pneumococcal polysaccharide vaccine, a 23-valent formulation, is recommended in children 2 years and older with an increased risk of invasive pneumococcal disease.36
Haemophilus Influenzae
Haemophilus organisms are small, nonmotile, gram-negative rods
that occur in both encapsulated and nonencapsulated forms. Approximately 90% to 95% of invasive disease is caused by the encapsulated sera type B. A pleural effusion or empyema is detected
in nearly 40% of patients with H. influenzae pneumonia. There is
an extremely high incidence of bacteremia in this disease. Serious
complications—such as epiglottitis, meningitis, and pericarditis—
can be diagnosed in 15% to 20% of patients. Cellulitis, anemia,
and septic arthritis occur infrequently.
In a hospitalized patient, administration of b-lactam agents
or a second- or third-generation cephalosporin is generally an

effective therapy.33,37 The mortality rate in appropriately treated
patients is generally considered to be less than 5% and often is
related to associated meningitis, epiglottitis, or pericarditis rather
than the pneumonic process itself. Hib conjugate vaccine is an
important measure in reducing the incidence of Haemophilusrelated disease and should be administered to all children.33,38,39

Staphylococcal Pneumonia
Primary S. aureus pneumonia has decreased in frequency in recent
years but still accounts for approximately 25% of cases in young
infants. The incidence of secondary or metastatic dissemination
has increased since 1972. Patients with primary pneumonia present
with fever and respiratory symptoms, whereas those with
metastatic disease often present with fever, generalized toxicity,
and musculoskeletal symptoms. In patients presenting with primary staphylococcal pneumonia, the disease is often preceded by
an upper respiratory tract infection.40 Pleural effusion or empyema develops in nearly 80% of the patients with primary staphylococcal pneumonia and is extremely common in patients with
metastatic disease. It is not unusual for patients with staphylococcal pneumonia to remain bacteremic long after the initiation of
appropriate antibiotic therapy.
Radiographic findings of S. aureus pneumonia differ according
to the stage of the disease. They vary from minimal changes to
consolidation (most common) and are associated with pleural effusion (50%–60%) or pneumothorax (21%). Pneumatoceles usually appear during the convalescent stage and may persist for
prolonged periods in asymptomatic patients. Antibiotic therapy
should be administered intravenously and include a drug that is
resistant to inactivation. Strong consideration should be given to
providing antibiotic coverage for methicillin-resistant S. aureus,
which can account for 1% to 30% of isolates depending on the
prevalence in the area.40 The duration of therapy is usually lengthier in patients with staphylococcal disease than for patients with
other bacterial pneumonias and consists of 21 days or more of
treatment. The mortality rate of staphylococcal pneumonia varies
from 23% to 33%. Increased mortality is usually associated with
younger age, inappropriate initial antimicrobial therapy, or failure
to drain an empyema appropriately.
Mycoplasma Pneumonia
Mycoplasma organisms are the smallest free-living microorganisms. They lack a cell wall and are pleomorphic. Mycoplasma is an
uncommon cause of pneumonia in children younger than 5 years
but is the leading cause of pneumonia in school-aged children and
young adults. Illness can range from a mild upper respiratory tract

infection to tracheobronchitis to pneumonia. Symptoms include
malaise, low-grade fevers, and headache. In 10% of children a
rash develops that usually is maculopapular. Cough, if it develops,
usually occurs within a few days and may continue for 3 to
4 weeks. Initially the cough is nonproductive but then may become productive and is usually associated with widespread rales
on physical examination. Radiographic abnormalities vary but are
usually bilateral and diffuse.41
Isolation of Mycoplasma by culture is complicated by the requirement for special enriched broth or agar media, which are
not widely available. It is successful in only 40% to 90% of cases
and requires 7 to 21 days. A fourfold increase in antibody titer
between acute and convalescent sera is diagnostic, but the time
involved is lengthy, providing only a retrospective diagnosis.
Complement fixation and immunofluorescent and several enzyme immunoassay antibody tests have been developed but are


CHAPTER 52  Pneumonitis and Interstitial Disease

of limited diagnostic value.33 Serum cold agglutinins with titers
of 1 : 32 or greater are present in more than 50% of patients
with pneumonia by the beginning of the second week of illness.
The PCR test has become an important means of diagnosing
M. pneumoniae infections in clinical practice, allowing for initiation of therapy directed at the causative pathogen.41 Treatment of
upper respiratory tract infections or acute bronchitis is rarely
indicated, but treatment with erythromycin or another macrolide,
such as azithromycin, is indicated for persons with pneumonia or
otitis media.

Gram-Negative Bacteria
Pneumonia caused by gram-negative enteric bacteria, especially
Pseudomonas, is almost always found in patients with underlying

pulmonary disease, compromised immune status, or those receiving prolonged respiratory therapy.42,43 Gram-negative enteric
bacteria are a frequent cause of nosocomial infection in critical
care units. These organisms can produce a severe necrotizing
pneumonia that is associated with an increase in morbidity.44

Legionella Pneumophila
Pneumonia caused by Legionella pneumophila has been reported
infrequently in the pediatric age group.45–48 The onset of this
disease is characterized by high, unremitting fever; chills; and a
nonproductive cough.46 Extrapulmonary manifestations include
gastrointestinal symptoms such as diarrhea, liver involvement,
and confusion. Chest radiographs typically consist of peripheral
nodular infiltrates and pleural effusions. Cavitation occurs only in
immunosuppressed individuals. Death in the normal host is unusual if prompt therapy with azithromycin or erythromycin is
initiated.
Anaerobic Bacteria
Pneumonia resulting from anaerobic upper respiratory flora is
uncommon in healthy children. When it does occur, it is frequently associated with risk factors such as underlying pulmonary
disease, a central nervous system (CNS) disorder (including seizures), a postanesthetic state, and aspiration of a foreign body.
Lung abscess and empyema are frequent complications in persons
with anaerobic bacterial pneumonias.

Complications
The mortality rate in persons with uncomplicated bacterial
pneumonia is less than 1%. Death is more common in children
with a complicated disease or an underlying disorder. The most
frequent complications of bacterial pneumonia are pleural effusion and empyema (Table 52.1). Thoracentesis should be performed if fluid is present to facilitate an etiologic diagnosis and
establish the character of the fluid. Tube thoracostomy is indicated if a large amount of fluid is present and causes respiratory
compromise or if purulent fluid is obtained by thoracentesis.
Empyema may extend locally to involve the pericardium, mediastinum, or chest wall. Evidence of empyema extension should

be considered in the child who is unresponsive to antibiotic
therapy.28
When tube thoracostomy/surgical drainage is required, it
should be discontinued as soon as drainage has substantially decreased. For patients with staphylococcal empyema, streptococcal
pneumonia, or H. influenzae empyema, 3 to 7 days of drainage is
usually sufficient. Patients with empyema require prolonged antimicrobial therapy and careful follow-up.

589

TABLE Major Sequelae/Life-Threatening Complications
52.1
Associated With Bacterial Infections

Complication/Sequelae

Organism

Necrotizing pneumonia

Anaerobic, GNB

Respiratory failure

GBS

Shock

GBS, SP, H. influenzae, GNB

Apnea

GBS

Pneumothorax

H. influenzae

Pneumatoceles

H. influenzae, anaerobic, staph, SP, GAS

Abscess (lung)

Staph, SP, anaerobic

Pleural effusion

H. influenzae, GAS, SP, staph

Empyema

H. influenzae, staph, SP

Epiglottitis

H. influenzae, GAS

Meningitis

H. influenzae, GBS, SP

Encephalopathy

Legionella

Pericarditis

H. influenzae

Bone/joint

H. influenzae, staph

Kidneys

Staph

GAS, Group A streptococcus; GBS, group B streptococcus; GNB, gram-negative bacteria;
SP, Streptococcus pneumoniae; staph, Staphylococcus aureus.

Pneumothorax and pneumatoceles can be seen with almost
any bacterial pneumonia but are especially common with
staphylococcal disease.49 Such pneumatoceles require no special
therapy and usually resolve. Lung abscess is an infrequent complication of H. influenzae and pneumococcal pneumonia and is
most often encountered with staphylococcal disease or anaerobic bacteria.
Prognosis is usually excellent, even in persons with severe bacterial pneumonia complicated by empyema. Long-term follow-up
of children with empyema has demonstrated remarkably few if
any residual pulmonary function abnormalities and remarkable
clearing of chest radiographs. In contrast to adults with empyema,
children seldom require surgical procedures such as decortication.

However, follow-up chest radiographs should be obtained on all
patients with bacterial pneumonia to document complete resolution. Such radiographic follow-up studies are probably not indicated until at least 6 to 8 weeks following the initiation of antibiotic therapy.

Therapy
Therapy for persons with bacterial pneumonia should include
appropriate IV antibiotic treatment directed toward the specific
pathogen if it is known (Table 52.2). Localized or compartmental complications—such as empyema, lung abscess, pericarditis, or septic joints—require appropriate surgical drainage
and antibiotic therapy. Prevention via immunization or chemoprophylaxis has changed the incidence and epidemiology of
pneumonitides significantly. Options for immunization, active
or passive, and chemoprophylaxis for various etiologic agents
are listed in Table 52.3.


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TABLE
Bacterial Pneumonia Therapy
52.2

Disease/Organism

Therapy

Undetermined Organisms
Serious, life-threatening pneumonia, nonsuppressed host

Cefotaxime or ceftriaxone 1 azithromycin 1 vancomycin
Bronchial lavage or needle aspiration of lung may be necessary to establish diagnosis.

Suppressed neutropenic host

Imipenem/meropenem or piperacillin or ceftazidime 1 aminoglycoside 6 clindamycin
Vancomycin not included in initial therapy unless high suspicion or if patient has indwelling
line. Amphotericin not used unless still febrile after 3 days/high suspicion. Bronchial lavage,
needle/open biopsy may be necessary to establish diagnosis.

Lung abscess

Clindamycin or ticarcillin/clavulanate or piperacillin/tazobactam

Specific Organisms
Pneumonia With Empyema
Streptococcus pneumoniae, group A strep
Penicillin susceptible

Preferred: ampicillin or penicillin 1 chest tube drainage
Alternative: ceftriaxone or cefotaxime 1 chest tube drainage

Penicillin resistant

Preferred: ceftriaxone 1 chest tube drainage
Alternative: ampicillin (increased dosing), levofloxacin or linezolid 1 chest tube drainage

Staphylococcus
Methicillin sensitive

Preferred: cefazolin, nafcillin or oxacillin 1 chest tube drainage
Alternative: clindamycin or vancomycin 1 chest tube drainage

Methicillin resistant

Preferred: vancomycin 1 chest tube drainage
Alternative: linezolid 1 chest tube drainage

Pneumonia Without Empyema
Haemophilus influenzae

Preferred: ampicillin or cefotaxime or ceftriaxone
Alternative: ciprofloxacin or levofloxacin

Klebsiella pneumoniae

Meropenem until susceptibilities are available

Escherichia coli, Enterobacter

Aminoglycoside or cephalosporin

Legionella

Preferred: azithromycin or erythromycin
Alternative: ciprofloxacin or levofloxacin

Pseudomonas

Aminoglycoside 1 anti-Pseudomonas penicillin or aminoglycoside 1 ceftazidime

Mycoplasma pneumoniae

Preferred: azithromycin
Alternative: erythromycin or levofloxacin

TABLE
Preventive Measures
52.3

Organism

Immunization

Chemoprophylaxis

Cytomegalovirus

IVIG: prophylaxis in seronegative transplant recipients

Ganciclovir or valganciclovir

Haemophilus influenzae type B

Capsular polysaccharide vaccine or conjugate vaccine

Cefotaxime or ceftriaxone

Influenza

Inactivated virus produced in chicken embryos

Oseltamivir (A or B) or zanamivir (A or B)

Measles

Live virus vaccine or IVIG for immunocompromised patients

None

Streptococcus pneumoniae

Capsular polysaccharide antigens of 13 or 23 pneumococcal
serotypes vaccine or pneumococcal conjugate vaccine

Penicillin VK for functional or anatomic asplenia until
age 5 y

Pneumocystis carinii

None

Trimethoprim-sulfamethoxazole or pentamidine or
dapsone or atovaquone

RSV

Palivizumab (monoclonal antibody)

None

Group B strep

None

Intrapartum antibiotics

IVIG, Intravenous immunoglobulin; RSV, respiratory syncytial virus; strep, Streptococcus spp.