Community-acquired Pneumonia
Community-acquired Pneumonia: Excerpt from Pediatric Infectious Disease
Epidemiology
Certain generalizations regarding the etiology of pediatric pneumonia can be
made. Viruses cause most lower respiratory diseases in younger children and
include respiratory syncytial virus, influenza A and B, parainfluenza, and
adenovirus. Respiratory syncytial virus and influenza viruses have their peak
incidence in the fall and winter months, whereas parainfluenza dominates in the
spring and summer. The presence of wheezing is more common in patients with
viral pneumonia as compared with bacterial disease. Bacterial pathogens
commonly associated with pneumonia include
Streptococcus pneumoniae, nontypeable Haemophilus influenzae, and Moraxella catarrhalis. Many clinicians consider bacterial pneumonia, particularly S. pneumoniae, to be the likely cause of lower respiratory infection if the clinical history
is characterized by acute onset of symptoms such as cough and high fever. In
regard to the atypical pathogens, there is an age-related decline in the
incidence of viral pneumonia accompanied by an increased incidence of these
infections as children approach adolescence.
Presentation
Recent reviews have suggested that the presence of an increased respiratory rate
may be the best method to distinguish lower respiratory tract infection from
the more common upper respiratory tract infections. The World Health
Organization has issued guidelines for the clinical diagnosis of pneumonia in
developing countries; the guidelines state that tachypnea and intercostal
retractions are the best indications of lower respiratory tract disease.
Diagnosis
Basic Diagnostic Approach
The proportion of children with pneumonia who are diagnosed with a specific
etiology is low. Unlike adults, children usually do not produce adequate sputum
specimens for Gram stain and culture. Blood cultures have a yield of less than
10% in patients with bacterial pneumonia.
“Lung puncture” studies that are conducted in developing countries are obviously not met with
enthusiasm in general pediatric practices. Prospective studies that have
employed sensitive antibody tests and polymerase chain reaction techniques have
suggested that in up to 20% of pediatric community-acquired pneumonias, the
infection is
“mixed” (i.e., both
S. pneumoniae and M. pneumoniae or C. pneumoniae); in these cases, the primary pathogen is not clear. Authors of these studies
have also suggested that mixed infection with bacteria and respiratory viruses
is likely to be common as
well.
Laboratory Findings
Many studies have looked at causes of pediatric pneumonia as it relates to
certain readily available laboratory measurements. Many clinicians consider
S. pneumoniae to be the likely cause of the lower respiratory infection if the picture is
characterized by acute onset of high fever, lobar pneumonia on chest
radiograph, leukocytosis, and a rapid response to
β-lactam antibiotics. Numerous studies have found that chest radiographs do not
readily distinguish between bacterial, atypical bacterial, and viral pneumonia.
A variety of laboratory tests have been used in the attempt to distinguish
bacterial from viral pneumonia, including the C-reactive protein and absolute
neutrophil counts. One problem in using
“screening” tests is that specific cutoff levels have often not been established. A recent
study done in Europe found that although white blood cell count and C-reactive
proteins were statistically higher in patients with pneumococcal infections,
other clinical and laboratory and radiographic studies were of little value.
Given the clinical, epidemiologic, and laboratory difficulties in pinpointing
the cause of pediatric pneumonia, an additional approach is to divide patients
by age.
Neonatal Pneumonia
Etiology
The primary bacterial pathogen in neonatal pneumonia is group B streptococci,
although
Escherichia coli and Listeria monocytogenes have also been reported. The mechanism is similar to that in neonatal sepsis,
where colonization from the mother results in neonatal colonization and
breakthrough infection.
Chlamydia trachomatis is the most common sexually transmitted infection in the United States. The
organism may reside in the genital tract of pregnant women and be transmitted
in about 60% of cases to infants at the time of delivery. About one half of
infants who acquire the organism develop conjunctivitis, and 20% eventually
develop lower respiratory disease.
Presentation
Pneumonia caused by bacteria such as group B streptococcus typically occurs in
the first weeks of life, presenting with fever, increased work of breathing,
and hypoxia.
C. trachomatis infection usually occurs between 2 and 19 weeks after birth. The infants are
afebrile, have increased respiratory rate, and cough. Children with chlamydial
pneumonia often have hyperinflation, and bilateral infiltrates on chest x-ray,
eosinophilia, and elevated serum immunoglobulin levels.
Diagnosis
Cultures of the blood, urine, and even cerebrospinal fluid are often obtained
and intravenous antibiotic started.
C. trachomatis can be diagnosed by culture or direct fluorescent antibody staining of
nasopharyngeal secretions.
Management
The management of the febrile tachypneic neonate suspected of having pneumonia
is similar to that of neonatal fever. Empiric intravenous antibiotics are
started until culture results are final. Empiric treatment usually consists of
ampicillin combined with gentamicin or a third-generation cephalosporin.
Treatment of
C. trachomatis is with oral erythromycin, 50 mg/kg per day in four divided doses for 2 weeks.
In the past, erythromycin was given to neonates exposed to
C. trachomatis at the time of delivery. Recently, there has been an association reported
between oral erythromycin and the subsequent development of hypertrophic
pyloric stenosis in infants younger than 6 weeks of age. The current
recommendation is to treat with oral erythromycin, 50 mg/kg per day in four
divided doses for 14 days all infants with chlamydial conjunctivitis and
pneumonia. Patients who are exposed at the time of delivery are not
presumptively treated, but rather monitored closely for the development of
disease. Routine screening of all pregnant women for sexually transmitted
disease is helpful in reducing disease by
C. trachomatis.
Pneumonia in the First 3 Months of Life
Respiratory Syncytial Virus
The peak incidence of this viral pathogen is in the first 6 months of life.
Respiratory syncytial virus (RSV) typically occurs annually during the winter
months. The spectrum of disease includes significant bronchiolitis and
pneumonia in infants and younger children to a mild upper respiratory infection
in older children. Patients with underlying conditions such as bronchopulmonary
dysplasia, congenital heart disease, or underlying immunodeficiency are at risk
for a more severe course.
RSV is diagnosed rapidly using a direct fluorescent antibody on nasal
secretions. An aerosolized antibiotic agent, ribavirin, has been used in the
treatment of RSV disease in infants. The use of ribavirin remains the subject
of continuing debate. Citing new evidence, the American Academy of Pediatrics
changed its recommendation in the 1990s regarding the use of ribavirin and now
has a less stringent
“may be considered” recommendation for its use in RSV infections in children with underlying
conditions such as immunodeficiency, congenital heart disease, or chronic lung
disease. Children with less serious disease need only supportive treatment.
Parainfluenza Virus
Parainfluenza viruses are very similar to the disease caused by RSV infection,
but usually seen in the summer months. These viruses frequently cause croup but
may also cause lower respiratory disease.
Streptococcus pneumoniae Infection
S. pneumoniae is the most common cause of bacterial pneumonia in this age group. This pathogen
is often associated with sudden onset of cough and high fever. Leukocytosis is
often present. Radiographs can show a discrete lobar pneumonia or round
infiltrate; this in the proper clinical context suggests the diagnosis.
Pertussis
Pertussis is seen in this age group owing to absent or incomplete immunizations.
Patients can present first with coryza (catarrhal stage) and then progress to
cough (paroxysmal stage). Infants may also present with apnea or seizures.
Lymphocytosis is frequently seen. The organism is difficult to culture and
often not present during the paroxysmal phase of the illness. The diagnosis is
made by direct immunofluorescence or polymerase chain reaction of nasal
secretions. Treatment is with erythromycin. Newer macrolide antibiotics can be
used, although there is less experience with these drugs.
Pneumonia in Children 4 Months to 5 Years of Age
Viral pathogens again predominate in this age group, with RSV, parainfluenza,
influenza, and adenovirus being common pathogens. The primary bacteria causing
pneumonia in infants and children remains
S. pneumoniae. Some studies also report M. catarrhalis, and nontypeable H. influenzae as pathogens.
Pneumonia in Children 5 Years of Age and Older
In this age group, the atypical pneumonias begin to be important agents. S. pneumoniae also remains a major cause of lower respiratory infection in this age group.
M. pneumoniae may begin with an upper respiratory infection that gradually progresses to
pneumonia. Cough is frequently a persistent symptom. Although
M. pneumoniae is classically a respiratory infection, additional extrapulmonary manifestations are seen and include encephalitis, hemolytic anemia, and Stevens-Johnson syndrome. Serology is usually the method for diagnosis.
C. pneumoniae was formerly termed TWAR strain. A sore throat or history of hoarseness usually
precedes the onset of lower respiratory infection and can be a clue to
diagnosis. Illness may run a protracted course lasting several weeks. The
diagnosis of the
C. pneumoniae is made by serology.
L. pneumophila is another pathogen associated with the atypical pneumonia group. Outbreaks are
often associated with exposure to water contaminated by the organism because it
tends to grow in water systems and air conditioning.
Legionella species are difficult to culture; it needs special buffer charcoal yeast
extract (BCYE agar) to support growth in the laboratory. Laboratories should
always be informed if
Legionella species infection is suspected. Patients who are hospitalized with severe
disease can undergo bronchoscopy for culture of bronchial alveolar fluids. In
addition to serology, direct fluorescent antibodies of bronchial alveolar
washings and urinary antigen testing are also available for diagnosis.
The atypical pathogens are treated differently from the other bacterial
pneumonias, relying on the use of either tetracycline or macrolide antibiotics.
Efforts have been made to devise a clinical scoring system that will identify
the atypical pathogen in the moderate to severely ill patient with
community-based pneumonia. Some studies have found high temperature and
previous unsuccessful therapy with
β-lactam antibiotics as being predictive of atypical pneumonia. Other studies
have not been able to differentiate reliably between the two groups of lower
respiratory infection. If there is a concern regarding etiology in a moderately
to severely ill patient, specific testing by serology, urinary antigen, or
bronchoscopy is advised.
Treatment of Community-acquired Pneumonia
The evaluation and empiric treatment of pediatric community-acquired pneumonia
has been the subject of numerous reviews. Investigators agree that clinical
evaluation forms the foundation for practice. If a child is nontoxic and has
obvious signs of a viral infection (such as rhinorrhea and nonexudative
pharyngitis), no antibiotics are required, and close follow-up is advocated.
In a young child who is suspected of having a bacterial illness (i.e.,
persistent fever), but who has good hydration status and adequate oxygenation,
empiric antibiotics are appropriate. Treatment with oral antibiotics is usually
directed against
S. pneumoniae because this is the most common cause of bacterial pneumonia in children.
During the past decade, alterations in penicillin-binding proteins have led to
increasing resistance of the pneumococci to both penicillin and the
cephalosporins. Increasing minimal inhibitory concentration (MIC) to
β-lactam antibiotics has resulted in new recommendations for the treatment of S. pneumoniae meningitis. Lower respiratory infection differs from meningitis in that there
is no blood
–brain barrier and therefore no reduction of antibiotic concentration in the
infected space. The MIC of
S. pneumoniae can thus be interpreted differently in pneumonia than in meningitis. In regard
to penicillin,
S. pneumoniae is reported as susceptible (MIC <= .06 µg/mL), intermediate (0.12 to 1.0 µg/mL), and resistant (>2.0 µg/mL). Unlike the therapy of meningitis, lower respiratory infections caused by
intermediate strains will usually respond to penicillin and other
β-lactam antibiotics. Pneumonia caused by resistant strains may not be
effectively treated by penicillin or even third-generation cephalosporins. In
these cases, alternate agents such as vancomycin or fluoroquinolones may be
required. An
S. pneumoniae isolate with an MIC to cefotaxime of 2.0 µg/mL or less can be treated with a third-generation cephalosporin.
In children older than 5 years of age, consideration of M. pneumoniae is required. Empiric treatment with a macrolide has been proposed for this age
group. Pneumococcal resistance to macrolide antibiotics is also increasing,
with two separate mechanisms of resistance identified.
S. pneumoniae resistance to macrolide may be secondary to alterations in drug-binding sites
or the development of active drug efflux. Although the overall
in vitro resistance rate of S. pneumoniae to macrolides approaches 30%, it is not clear whether this correlates with
clinical failure. It has been suggested that the clinical effect of
in vitro macrolide resistance may depend on the precise mechanism of resistance present
in the infecting organism or the presence of concurrent bacteremic disease.
Macrolide therapy for presumed
S. pneumoniae lower respiratory disease is reasonable in a stable outpatient population;
children who are toxic, bacteremic, or fail to improve after macrolide
monotherapy may warrant combination therapy with
β-lactam antibiotics.
In children who are toxic appearing, hypoxic, or require intravenous hydration,
treatment is directed toward both atypical pathogens and bacteria causing
severe pyogenic pneumonia, including
Streptococcus pyogenes, S. pneumoniae, and Staphylococcus aureus. In treating pneumonia in a toxic-appearing child, the clinician must remember
the increasing incidence of resistance in both community
S. aureus (MRSA) and S. pneumoniae (MIC to penicillin $gt;= 2.0 µg/mL). Vancomycin and a third-generation cephalosporin are reasonable initial
therapy in the case of a potentially life-threatening lower respiratory
infection. For children who are not in critical condition, a third-generation
cephalosporin, clindamycin, or ampicillin-sulbactam (Unasyn) is an acceptable
choice. A macrolide antibiotic will also be needed for treatment of the
atypical pneumonia pathogens (Table 13.1).
Parapneumonic Effusions and Empyema
Bacterial pneumonia can have a variety of complications. A parapneumonic
effusion refers to pleural fluid that accumulates in association with bacterial
pneumonia. A certain percentage of these effusions will undergo a secondary
process in which the fluid becomes purulent and, if untreated, will actually
form a pleural peel that adheres to the surface of the lung. At this stage, the
parapneumonic effusion is typically referred to as an
empyema.
Etiology
The three major bacteria responsible for parapneumonic effusion and empyema are S. aureus, S. pneumoniae, and S. pyogenes (group A streptococci). The rate of empyema varies with each particular
bacterium; group A streptococcus pneumonia progresses to empyema in up to 40%
of patients, whereas less than 5% of patients with pneumococcal pneumonia
develop an empyema.
Clinical and Radiographic Features
Patients with parapneumonic effusions or empyema often continue to have spiking
temperatures despite appropriate antibiotics. Chest x-ray is usually the
initial step in evaluating this condition. If there is extensive effusion, the
chest radiograph may appear as a
“whiteout,” the entire side of the lung becomes opaque. In these cases, computed tomography
of the chest is excellent in distinguishing pleural from parenchymal disease.
Computed tomography can also detect the presence of large loculations (Figs.
13.1 and 13.2).
Diagnosis
Once a pleural effusion has been identified, analysis of the pleural effusion is
necessary. A common mistake is to delay evaluation and drainage of pleural
effusion; this can ultimately lead to further formation of loculations and
greater difficulty in ultimately clearing the infection.
Because treatment of empyema requires not only antibiotic therapy but also
surgical drainage, there is great interest in the pleural fluid parameters that
define the diagnosis of empyema. Aspiration of frankly purulent material, a
positive Gram stain, or positive pleural culture is enough to make a definitive
diagnosis. In the absence of frankly purulent material, there are changes that,
of themselves, warrant consideration for drainage. A pleural fluid pH of less
than 7.2, a glucose level of less than 40 mg/dL, and a lactate dehydrogenase
(LDH) level of more than 1,000 IU identify a complicated parapneumonic effusion
that requires drainage.
Pleural fluid should be obtained under sterile conditions and sent for a variety
of specific tests. It should be plated on both aerobic and anaerobic media.
Determination of the pH of the pleural fluid is vital and should be collected
anaerobically and transported on ice to the laboratory. Cell count and chemical
analysis are also important.
Management
Treatment of Empyema
In patients in whom an empyema is diagnosed, either by pH, LDH, glucose, Gram
stain, or the documentation of gross pus within the pleural space, at the very
least a chest tube is required for continued drainage. If the initial suspicion for
empyema is high, initial diagnostic thoracentesis may be replaced by immediate
placement of a chest tube. In most cases, chest tubes can be removed when the
amount of pleural fluid draining from the tube has decreased and the effusion
has resolved on plain x-ray. There will be a percentage of patients who do not
clear the empyema with chest tube drainage alone. These patients are candidates
for further surgical intervention. Patients who require surgical intervention
typically have persistent fever, toxicity, and minimal chest tube drainage.
These patients often have developed loculations that are not amenable to
drainage by chest tube.
In the past, thoracotomy and decortication was done. In this procedure, the
chest is
opened, pleura removed, and purulent material evacuated from the pleural space.
Video-assisted thoracic surgery (VATS) is being increasingly used; this
procedure has the advantage of a smaller surgical incision and fewer
complications. A greater number of pediatric surgeons are advocating earlier
use of VATS, even before placement of a chest tube, for the initial treatment
of pediatric empyema. As experience with VATS increases, it may be prudent to
involve an experienced pediatric surgeon as soon as a pleural empyema is
diagnosed (Table 13.2).
Selected Readings
Campbell JD, Nataro JP. Pleural empyema. Pediatr Infect Dis J 1999;18(8):725–726.
Gaston B. Pneumonia. Pediatr Rev 2002;23(4):132–140.
McCracken GH. Diagnosis and management of pneumonia in children. Pediatr Infect Dis J 2000;(9):
924–928.
Rodriguez JA, Hill CB, Loe WA, et al. Video-assisted thoracoscopic surgery for
children with stage II empyema.
Am Surg 2000;66(6):569–572.
Pictures
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Book Source Details
- Book Title: Pediatric Infectious Disease
- Author(s): Donald Janner MD
- Year of Publication: 2004
- Copyright Details: Pediatric Infectious Disease, Copyright © 2004 Lippincott Williams & Wilkins.
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More About This Book:
Title: Pediatric Infectious Disease
Authors: Donald Janner MD
Publisher: Lippincott Williams & Wilkins
Copyright: 2004
ISBN: 0-7817-5584-0
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