Neonatal Pneumonia

Official reprint from UpToDate
www.uptodate.com
Print | Back
INTRODUCTION - Pneumonia is an important cause of neonatal infection and accounts for
significant morbidity and mortality, especially in developing countries [1,2]. In these countries,
the World Health Organization estimates that almost 800,000 neonatal deaths occur each year
from acute respiratory infections, mostly pneumonia [3]. In a rural area in central India, for
example, mortality secondary to pneumonia in the first month was 29 per 1000 live births; more
than one-half of all pneumonia deaths in children occurred in newborns [4]. These figures may be
an underestimate because many newborns do not receive medical care.
In developed countries, the estimated incidence of pneumonia in full-term infants is less than 1
percent. However, among ill infants of normal and low-birth-weight, the incidence may be closer
to 10 percent [5].
By contrast at autopsy, the incidence of neonatal pneumonia ranges from 20 to 32 percent of live-
born and from 15 to 38 percent of stillborn infants, although the pathologic features of
inflammation of the lung may not always result from infection [6]. In one series, infection was the
most common etiology of death in extremely low-birth-weight infants (56 of 111); congenital
pneumonia accounted for 30 of these 56 infections [7]. Pneumonia caused by maternal enteric
organisms frequently accompanies chorioamnionitis and/or funisitis in these congenital infections.
The pathogenesis, clinical manifestations, diagnosis, and treatment of neonatal pneumonia are
reviewed here. Neonatal sepsis and specific pathogens are discussed separately. (See related
topics).
PATHOGENESIS - Neonatal pneumonia can have early or late onset. Bacteria are the principal
pathogens for both types. (See 'Microbiology' below.)
Routes of acquisition - The route of acquisition varies in part with the time of onset of the
pneumonia.
Early-onset pneumonia - Early-onset pneumonia, generally within three days of birth, is
acquired from the mother by one of three routes:
Intrauterine aspiration of infected amniotic fluid
Transplacental transmission of organisms from the mother
to the fetus through the placental circulation
Aspiration during or after birth of infected amniotic fluid.
The neonate also can aspirate vaginal organisms, leading to respiratory colonization and, in some
cases, pneumonia. Vaginal colonization with such organisms as group B streptococcus (GBS) does
not necessarily result in overt maternal infection.
Late-onset pneumonia - Late-onset pneumonia, which occurs during hospitalization or after
discharge, generally arises from organisms colonizing the hospitalized newborn or is nosocomially
acquired from infected individuals or contaminated equipment. Microorganisms can invade
through injured tracheal or bronchial mucosa or through the bloodstream.
Mechanism of injury in GBS pneumonia - In GBS pneumonia, the level of beta-hemolysin
Neonatal pneumonia

Last literature review for version 17.3: septiembre 30, 2009 | This topic last updated:
agosto 11, 2009
Author
Michael E Speer, MD
Section Editors
Joseph A Garcia-Prats, MD
Morven S Edwards, MD
Deputy Editor
Melanie S Kim, MD
Page 1 oI 11 Neonatal pneumonia
13/03/2010 http://www.uptodate.com/online/content/topic.do?topicKeyneonatol/2537&viewprint
expression appears to correlate directly with the ability of the organism to injure lung epithelial
cells [8,9]. Studies suggest the hemolysin acts as a pore-forming cytolysin. The injury results in
increased permeability that contributes to the development of alveolar edema and hemorrhage.
This mechanism also may be partially responsible for bloodstream extension. Because surfactant
phospholipid inhibits beta-hemolysin-associated lung epithelial cell injury, premature infants who
are deficient in surfactant may be more severely affected [8,9].
Pathology - The pathologic changes vary with the type of organism: bacterial or viral. Bacterial
pneumonia is characterized by inflammation of the pleura, infiltration or destruction of
bronchopulmonary tissue, and leukocyte and fibrinous exudate within alveoli and the
bronchi/bronchioles [10,11]. Bacteria often are seen within the interstitial spaces, alveoli, and
bronchi/bronchioles [10].
Viruses typically cause an interstitial pneumonia. The pneumonia induced by rubella, for example,
is characterized by infiltration of mononuclear cells and lymphocytes. Extensive inflammation
occasionally occurs with hyaline membrane formation, followed by varying degrees of interstitial
fibrosis and scarring [12-14].
MICROBIOLOGY - Bacterial, viral, spirochetal, protozoan, and fungal pathogens can cause
pneumonia.
Early-onset pneumonia - Bacterial pathogens are the most common cause of early- and late-
onset pneumonia, although the specific organisms may differ (table 1).
Bacterial infections - Most early-onset pneumonia is caused by aerobic bacteria, although
anaerobes such as Bacteroides sp. occasionally are recovered. GBS causes most early-onset
disease in the United States [15], Great Britain [16], and other developed countries [17,18]. (See
"Group B streptococcus: Virulence factors and pathogenic mechanisms" and "Group B
streptococcal infection in neonates and young infants".) In one study from the United Kingdom of
35 infants with early-onset pneumonia, GBS was responsible for 57 percent of the cases [16].
Different organisms may predominate in other locations, especially developing countries
[2,5,19,20]. In a review of neonatal pneumonia in developing countries, pathogens responsible for
early onset neonatal sepsis and pneumonia included Escherichia coli, group B Streptococcus,
Klebsiella spp, Staphylococcus aureus, and Streptococcus pneumoniae [2].
Other less common bacterial pathogens include Listeria monocytogenes and Mycobacterium
tuberculosis, both of which can be transmitted transplacentally. Although transplacental infection
by M. tuberculosis often results in primary liver involvement, pneumonia may be the sole
manifestation or may accompany hepatic disease [21]. Tuberculosis (TB) occurs with greater
frequency in human immunodeficiency virus (HIV)-infected patients, and congenital TB also has
become more common [22].
Possible link of Ureaplasma urealyticum to chronic lung disease - One bacterial
pathogen, Ureaplasma urealyticum, has been linked potentially to the development of acute and
chronic lung disease [23-27]. This connection has been shown in both small series and a meta-
analysis [24].
In one study of 47 infants weighing <1500 g, radiographic features of pneumonia were more
frequent within seven days in those colonized with U. urealyticum than in noncolonized infants (53
versus 21 percent) [23]. Evidence of "precocious" chronic lung disease by radiography also was
more common in patients with a positive culture for the organism (23 versus 2 percent). Infants
with a positive U. urealyticum culture had a relative risk of 11.0 (95% CI 1.6 -75.5) for
oxygen dependence at 36 postmenstrual weeks [23].
In another report, tracheal aspirates were obtained prior to administration of surfactant or
antibiotics from 105 very low-birth-weight infants who required mechanical ventilation before 12
hours of age [25]. Infants positive for U. urealyticum were more likely to have chronic lung
disease at 28 days but not at 36 postmenstrual weeks [25].
The efficacy of antimicrobial therapy is uncertain. Two small trials of erythromycin therapy in
colonized infants failed to show an effect on the development of chronic lung disease [26,27].
Viral infections - Herpes simplex virus (HSV) is the most common viral agent to cause early-
onset pneumonia, usually following acquisition from the mother at the time of birth [28]. HSV
pneumonia occurs in 33 to 54 percent of disseminated HSV infections and usually is fatal in spite
of treatment [28,29].
Other viruses can cause pneumonia, usually via transplacental transmission from a mother who
acquires the infection late in pregnancy. Examples include adenovirus, enteroviruses, and mumps
[29-31]. Interstitial pneumonitis also frequently occurs in congenital rubella infection, although
this is an uncommon manifestation of congenital cytomegalovirus (CMV) infection, occurring in
less than 1 percent of cases [32,33].
Fungal infections - Candida sp. and other fungal pathogens also are responsible for neonatal
pneumonia [34,35]. In one prospective study, approximately 25 percent of very low-birth-weight
infants were colonized by Candida in the gastrointestinal and respiratory tracts, presumably during
labor and delivery [36]. Pneumonia occurs in approximately 70 percent of infants with systemic
candidiasis [37].
Other pathogens - Occasionally, early-onset pneumonia is seen in patients with congenital
toxoplasmosis and syphilis [38].
Late-onset pneumonia - Hospitalized infants often are colonized with organisms that are
different from normal flora and that can cause late-onset pneumonia.
Bacterial infections - There is limited information on the bacterial etiology for community
acquired, late onset pneumonia [2]. There appears to be a predominance of gram positive
bacteria including S. pyogenes, S. aureus, and S. pneumoniae. Other bacterial pathogens have
been implicated in late-onset pneumonia; some of which have characteristic features:
Staphylococcus aureus and Klebsiella pneumoniae are notable for inducing extensive tissue
damage, abscess formation, and empyema [39].
These and other pathogens (eg, Escherichia coli, Serratia marcescens, Enterobacter cloacae,
Streptococcus pneumoniae, and Pseudomonas aeruginosa) may cause pneumatoceles [40-42].
Citrobacter diversus, frequently associated with brain abscesses in neonates, can cause lung
abscess [40].
Bacillus cereus has been associated with necrotizing pneumonia in preterm infants [43] and
with pneumonia secondary to contaminated ventilator circuits [44].
Chlamydia trachomatis has a long incubation period and typically is associated with
pneumonia occurring between two and four weeks of age [45]. A possible association between
early lung disease and a positive tracheal culture for C. trachomatis has been reported [46]. In
developing countries where untreated sexually transmitted is common, C. trachomatis nasal
carriage rate is between 15 to 20 percent and is a risk factor for pneumonia [2,19,47].
Viral infections - Numerous viruses, including adenovirus, parainfluenza, rhinovirus,
enteroviruses, influenza, and respiratory syncytial virus (RSV), cause pneumonia in the neonatal
period [29,48,49]. Most infants initially are healthy but have ill family members. In a series of 40
newborns with viral pneumonia, nine were born at less than 37 weeks gestation, and RSV
accounted for 55 percent of the cases [48]. RSV is most prevalent during the winter months and
results in significant morbidity and mortality.
Fungal infections - Candida sp. occasionally cause late-onset pneumonia, particularly in
extremely low-birth-weight infants who have received prolonged antibiotic therapy and have
respiratory tract colonization [5,50-52]. Corticosteroid administration may increase the risk of
systemic infection from Candida sp. in premature infants [53,54], potentially increasing the risk of
pneumonia.
A rare cause of pneumonia is aspergillosis which frequently is fatal [55]. Aspergillus infection can
occur in clusters, particularly during hospital renovations [56].
RISK FACTORS - Risk factors associated with early-onset pneumonia include prolonged rupture
of the fetal membranes (>18 hours), maternal amnionitis, premature delivery, fetal tachycardia,
and maternal intrapartum fever [15,17,29].
Infants who require assisted ventilation are at highest risk for late-onset pneumonia. Data from
adults, which are thought to be applicable to neonates, suggest that the risk of nosocomial
pneumonia is approximately four times higher in intubated than in nonintubated patients [57].
Other risk factors include:
Anomalies of the airway (eg, choanal atresia, tracheoesophageal fistula, and cystic
adenomatoid malformations)
Severe underlying disease
Prolonged hospitalization
Neurologic impairment resulting in aspiration of gastrointestinal contents.
Nosocomial infections occasionally are traced to poor handwashing or overcrowding [58].
CLINICAL MANIFESTATIONS - Early-onset pneumonia commonly presents with respiratory
distress beginning at or soon after birth. Infants may have associated lethargy, apnea,
tachycardia and poor perfusion, sometimes progressing to septic shock. Some infants develop
pulmonary hypertension. Other signs include temperature instability, metabolic acidosis, and
abdominal distension. None of these signs is specific for pneumonia, and respiratory distress also
can be caused by noninfectious causes (table 2).
Late-onset pneumonia is marked by changes in the overall condition of the newborn and can
include nonspecific signs of apnea, tachypnea, poor feeding, abdominal distention, jaundice,
emesis, respiratory distress, and circulatory collapse. Ventilator-dependent infants may have
increased oxygen and ventilator requirements or purulent tracheal secretions.
DIAGNOSIS - Because signs of pneumonia are nonspecific, any newborn infant with sudden
onset of respiratory distress or other signs of illness should be evaluated for pneumonia and/or
sepsis.
Cultures - Cultures of blood and cerebrospinal fluid should be obtained. Pleural fluid, if present
in a sufficient volume, can be cultured. If viral or other nonbacterial infection is suspected, specific
studies should be obtained. Gram stain and culture of tracheal aspirates may identify the
causative organism.
In one study, aspirates were obtained from 320 high-risk infants within eight hours of birth,
either by tracheal suctioning under direct visualization or immediately following intubation [59].
Organisms were isolated from culture in 14 of the 25 (56 percent) who had bacteria present in the
smear of the aspirate.
In another series of 28 intubated infants, the presence of both polymorphonuclear leukocytes
and bacteria in tracheal aspirates correlated well with pneumonia [60].
Surveillance tracheal aspirate cultures may provide early information about possible pathogens
when sepsis occurs, and diagnosing pneumonia [61-63]. Needle aspiration or bronchoscopy is
difficult to perform in sick newborns and may have significant morbidity [5].
Chest radiography - The chest radiograph can confirm the clinical diagnosis of pneumonia.
Bilateral alveolar densities with air bronchograms are characteristic [64], but irregular patchy
infiltrates or occasionally a normal pattern also occur [65]. Pneumonia caused by GBS or other
pathogens is difficult to distinguish from respiratory distress syndrome in premature infants [66-
68]. The presence of pleural effusions may be helpful because they occur in up to 67 percent of
patients with pneumonia but are rarely found in respiratory distress syndrome. However, pleural
effusions also can be seen in patients with transient tachypnea of the newborn, congenital heart
disease, hydrops fetalis, and congenital lymphangiectasia [65].
TREATMENT - Successful treatment depends upon the pathogen, early recognition of the
infection, and early therapy prior to the development of irreversible injury.
Bacterial infection - The choice of empiric regimens is based upon whether the infection is
early- or late-onset.
Early-onset pneumonia - For early-onset pneumonia, empiric parenteral antibiotic
treatment for maternal genital organisms is started until culture results are available. Once a
specific organism is identified, therapy is modified according to the susceptibility pattern.
A frequently used initial regimen for empiric coverage is ampicillin (150 mg/kg IV Q12h if
meningitis is suspected and 50 to 100 mg/kg IV Q12h if not) and gentamicin (dose based upon
gestational age and renal function). Ampicillin is effective against GBS, most other strains of
streptococci, L. monocytogenes, and some Gram-negative bacteria. Ampicillin plus gentamicin
also has synergistic activity against many of these organisms [69]. In institutions in which a
substantial proportion of nosocomial Gram-negative bacilli are resistant to gentamicin, another
aminoglycoside should be substituted.
Third generation cephalosporins, although active against many Gram-negative organisms, should
not be used for suspected sepsis or pneumonia. Gram-negative bacilli can rapidly develop
resistance to cephalosporins by either inducible or chromosomally mediated beta-lactamase
activity [69,70].
Late-onset pneumonia - The choice of empiric therapy for late-onset pneumonia depends
upon the prevalence and sensitivity of bacteria in both the community and the hospital. For term
infants more than three to five days old, vancomycin (30 mg/kg per day IV given in divided doses
Q8-12h) plus an aminoglycoside (dose based upon gestational age and renal function) is used as
initial therapy because of the high prevalence of staphylococcal species resistant to penicillins (eg,
Staphylococcus epidermidis and methicillin-resistant S. aureus [MRSA]). Because of the
emergence of vancomycin-resistant enterococci (VRE) and S. aureus with reduced susceptibility to
vancomycin, vancomycin should be continued only if there is no alternative [71]. Dosing of
vancomycin in the preterm infant should be determined by postnatal and gestational age.
If P. aeruginosa is suspected, an aminoglycoside plus ticarcillin with clavulanate is appropriate
therapy (dose is based upon the ticarcillin component at 75 to 100 mg/kg per dose ticarcillin
component administered every 8 to 12 hours) [69]. Tobramycin is particularly active against this
organism. Tobramycin dosing is based upon the patient's gestational age and renal function.
Ceftazidime is an alternative to ticarcillin-clavulanate.
The duration of therapy is guided by the infecting pathogen and the response of the patient. The
usual treatment course for uncomplicated pneumonia is 10 to 14 days.
Viral infections - Specific agents for the treatment of viral pneumonia are limited. For most
viral infections acquired in the perinatal or postnatal period, therapy remains supportive. (See
related topics).
Herpes simplex virus - If HSV pneumonia is suspected, intravenous acyclovir (60 mg/kg per
day in 3 divided doses for 21 days) is recommended [72]. HSV pneumonia usually is fatal despite
treatment [28,29].
Respiratory syncytial virus - Ribavirin is the only available treatment for RSV pneumonia,
although trials lack sufficient power to estimate effects reliably. A meta-analysis of randomized
trials of ribavirin in infants less than six months old showed that ribavirin reduced the duration of
ventilation by 1.2 days (95% CI -0.2 to -3.4) but did not reduce mortality [73].
High-risk infants (eg, those with chronic lung disease or born at less than 35 weeks gestation) can
receive preventive treatment for RSV. (See "Respiratory syncytial virus infection: Treatment and
prevention".)
OUTCOME - Although most neonates in developed countries do well, prognosis from neonatal
pneumonia is predicated upon the severity of the disease, the gestational age of the patient,
underlying medical conditions, and the infecting organism. Increased mortality is associated with
preterm birth, pre-existing chronic lung disease, or immune deficiencies.

Use of is subject to the Subscription and License Agreement.
REFERENCES

1. Stoll, BJ. The global impact of neonatal infection. Clin Perinatol 1997; 24:1.
2. Duke, T. Neonatal pneumonia in developing countries. Arch Dis Child Fetal Neonatal Ed
2005; 90:F211.
3. Garenne, M, Ronsmans, C, Campbell, H. The magnitude of mortality from acute respiratory
infections in children under 5 years in developing countries. World Health Stat Q 1992;
45:180.
4. Bang, AT, Bang, RA, Morankar, VP, et al. Pneumonia in neonates: Can it be managed in the
community? Arch Dis Child 1993; 68:550.
5. Dennehy, PH. Respiratory infections in the newborn. Clin Perinatol 1987; 14:667.
6. Barnett ED, MI, Klein, JO. Bacterial Infections of the Respiratory Tract. In: Infectious
Diseases of the Fetus and the Newborn, 6th ed, Remington, JS, Klein JO, Wilson, CB, Baker,
CJ (Eds), Elsevier Saunders, Philadelphia 2006, p 297.
7. Barton, L, Hodgman, JE, Pavlova, Z. Causes of death in the extremely low birth weight
infant. Pediatrics 1999; 103:446.
8. Nizet, V, Gibson, RL, Rubens, CE. The role of group B streptococci beta-hemolysin
expression in newborn lung injury. Adv Exp Med Biol 1997; 418:627.
9. Gibson, RL, Nizet, V, Rubens, CE. Group B streptococcal beta-hemolysin promotes injury of
lung microvascular endothelial cells. Pediatr Res 1999; 45:626.
10. Davies, PA, Aherne, W. Congenital pneumonia. Arch Dis Child 1962; 37:598.
11. Robbins, SL. The Respiratory System - Lung. In: Textbook of Pathology With Clinical
Application, WB Saunders, Philadelphia 1962. p.562.
12. Hanshaw, JB, Dudgeon, JA. Rubella. In: Viral Diseases of the Fetus and Newborn, WB
Saunders, Philadelphia 1978. p.17.
13. Singer, DB, Rudolph, AJ, Rosenberg, HS, et al. Pathology of the congenital rubella
syndrome. J Pediatr 1967; 71:665.
14. Korones, SB, Ainger, LE, Monif, GR, et al. Congenital rubella syndrome: New clinical aspects
with recovery of virus from affected infants. J Pediatr 1965; 67:166.
15. Revised guidelines for prevention of early-onset group B streptococcal (GBS) infection.
American Academy of Pediatrics Committee on Infectious Diseases and Committee on Fetus
and Newborn. Pediatrics 1997; 99:489.
16. Webber, S, Wilkinson, AR, Lindsell, D, et al. Neonatal pneumonia. Arch Dis Child 1990;
65:207.
17. Spaans, WA, Knox, AJ, Koya, HB, Mantell, CD. Risk factors for neonatal infection. Aust N Z J
Obstet Gynaecol 1990; 30:327.
18. Kalliola, S, Vuopio-Varkila, J, Takala, AK, Eskola, J. Neonatal group B streptococcal disease
in Finland: A ten-year nationwide study. Pediatr Infect Dis J 1999; 18:806.
19. Muhe, L, Tilahun, M, Lulseged, S, et al. Etiology of pneumonia, sepsis and meningitis in
infants younger than three months of age in Ethiopia. Pediatr Infect Dis J 1999; 18:S56.
20. Prasertsom, W, Horpaopan, S, Ratrisawadi, V, et al. Early versus late onset neonatal
septicemia at Children's Hospital. J Med Assoc Thai 1990; 73:106.
21. Starke, JR. Tuberculosis. An old disease but a new threat to the mother, fetus, and neonate.
Clin Perinatol 1997; 24:107.
22. Adhikari, M, Pillay, T, Pillay, DG. Tuberculosis in the newborn: An emerging disease. Pediatr
Infect Dis J 1997; 16:1108.
23. Pacifico, L, Panero, A, Roggini, M, et al. Ureaplasma urealyticum and pulmonary outcome in
a neonatal intensive care population. Pediatr Infect Dis J 1997; 16:579.
24. Wang, EE, Ohlsson, A, Kellner, JD. Association of Ureaplasma urealyticum colonization with
chronic lung disease of prematurity: Results of a metaanalysis. J Pediatr 1995; 127:640.
25. Perzigian, RW, Adams, JT, Weiner, GM, et al. Ureaplasma urealyticum and chronic lung
disease in very low birth weight infants during the exogenous surfactant era. Pediatr Infect
Dis J 1998; 17:620.
26. Lyon, AJ, McColm, J, Middlemist, L, et al. Randomised trial of erythromycin on the
development of chronic lung disease in preterm infants. Arch Dis Child Fetal Neonatal Ed
1998; 78:F10.
27. Bowman, ED, Dharmalingam, A, Fan, WQ, et al. Impact of erythromycin on respiratory
colonization of Ureaplasma urealyticum and the development of chronic lung disease in
extremely low birth weight infants. Pediatr Infect Dis J 1998; 17:615.
28. Barker, JA, McLean, SD, Jordan, GD, et al. Primary neonatal herpes simplex virus
pneumonia. Pediatr Infect Dis J 1990; 9:285.
29. Campbell, JR. Neonatal pneumonia. Semin Respir Infect 1996; 11:155.
30. Meyer, K, Girgis, N, McGravey, V. Adenovirus associated with congenital pleural effusion. J
Pediatr 1985; 107:433.
31. Groenendaal, F, Rothbarth, PH, van den, Anker JN, Spritzer, R. Congenital mumps
pneumonia: a rare cause of neonatal respiratory distress. Acta Paediatr Scand 1990;
79:1252.
32. Stagno, S. Cytomegalovirus. In: Infectious Diseases of the Fetus & Newborn, Remington,
JS, Klein, JO (Eds), WB Saunders, Philadelphia, 1995, p. 312.
33. Boppana, SB, Fowler, KB, Britt, WJ, et al. Symptomatic congenital cytomegalovirus infection
in infants born to mothers with preexisting immunity to cytomegalovirus. Pediatrics 1999;
104:55.
34. Ng, PC, Siu, YK, Lewindon, PJ, et al. Congenital Candida pneumonia in a preterm infant. J
Paediatr Child Health 1994; 30:552.
35. Gerberding, KM, Eisenhut, CC, Engle, WA, Cohen, MD. Congenital candida pneumonia and
sepsis: A case report and review of the literature. J Perinatol 1989; 9:159.
36. Baley, JE, Kliegman, RM, Boxerbaum, B, Fanaroff, AA. Fungal colonization in the very low
birth weight infant. Pediatrics 1986; 78:225.
37. Baley, JE, Kliegman, RM, Fanaroff, AA. Disseminated fungal infections in very low-birth-
weight infants: Clinical manifestations and epidemiology. Pediatrics 1984; 73:144.
38. Edell, DS, Davidson, JJ, Mulvihill, DM, Majure, M. A common presentation of an uncommon
cause of neonatal respiratory distress: Pneumonia alba. Pediatr Pulmonol 1993; 15:376.
39. Marks, MI, Klein, JO. In: Infectious Diseases of the Fetus & Newborn, Remington, JS, Klein,
JO (Eds), W B Saunders Company, Philadelphia 1995. p.899.
40. Shamir, R, Horev, G, Merlob, P, Nutman, J. Citrobacter diversus lung abscess in a preterm
infant. Pediatr Infect Dis J 1990; 9:221.
41. Khan, EA, Wafelman, LS, Garcia-Prats, JA, Taber, LH. Serratia marcescens pneumonia,
empyema and pneumatocele in a preterm neonate. Pediatr Infect Dis J 1997; 16:1003.
42. Glustein, JZ, Kaplan, M. Enterobacter cloacae causing pneumatocele in a neonate. Acta
Paediatr 1994; 83:990.
43. Jevon, GP, Dunne, WM Jr, Hicks, MJ, Langston, C. Bacillus cereus pneumonia in premature
neonates: A report of two cases. Pediatr Infect Dis J 1993; 12:251.
44. Gray, J, George, RH, Durbin, GM, et al. An outbreak of Bacillus cereus respiratory tract
infections on a neonatal unit due to contaminated ventilator circuits. J Hosp Infect 1999;
41:19.
45. Jain, S. Perinatally acquired Chlamydia trachomatis associated morbidity in young infants. J
Matern Fetal Med 1999; 8:130.
46. Colarizi, P, Chiesa, C, Pacifico, L, et al. Chlamydia trachomatis-associated respiratory
disease in the very early neonatal period. Acta Paediatr 1996; 85:991.
47. Lehmann, D, Sanders, RC, Marjen, B, et al. High rates of Chlamydia trachomatis infections
in young Papua New Guinean infants. Pediatr Infect Dis J 1999; 18:S62.
48. Abzug, MJ, Beam, AC, Gyorkos, EA, Levin, MJ. Viral pneumonia in the first month of life.
Pediatr Infect Dis J 1990; 9:881.
49. Palivizumab, a humanized respiratory syncytial virus monoclonal antibody, reduces
hospitalization from respiratory syncytial virus infection in high-risk infants. The IMpact-RSV
Study Group. Pediatrics 1998; 102:531.
50. Rowen, JL, Rench, MA, Kozinetz, CA, et al. Endotracheal colonization with Candida enhances
risk of systemic candidiasis in very low birth weight neonates. J Pediatr 1994; 124:789.
51. Loke, HL, Verber, I, Szymonowicz, W, Yu, VY. Systemic candidiasis and pneumonia in
preterm infants. Aust Paediatr J 1988; 24:138.
52. Narang, A, Agrawal, PB, Chakrabarti, A, Kumar, P. Epidemiology of systemic candidiasis in a
tertiary care neonatal unit. J Trop Pediatr 1998; 44:104.
53. Groll, AH, Jaeger, G, Allendorf, A, et al. Invasive pulmonary aspergillosis in a critically ill
neonate: case report and review of invasive aspergillosis during the first 3 months of life.
Clin Infect Dis 1998; 27:437.
54. Botas, CM, Kurlat, I, Young, SM, Sola, A. Disseminated candidal infections and intravenous
hydrocortisone in preterm infants. Pediatrics 1995; 95:883.
55. Rowen, JL, Atkins, JT, Levy, ML, et al. Invasive fungal dermatitis in the < or = 1000-gram
neonate. Pediatrics 1995; 95:682.
56. Krasinski, K, Holzman, RS, Hanna, B, et al. Nosocomial fungal infection during hospital
renovation. Infect Control 1985; 6:278.
57. Cross, AS, Roup, B. Role of respiratory assistance devices in endemic nosocomial
pneumonia. Am J Med 1981; 70:681.
58. Harbarth, S, Sudre, P, Dharan, S, et al. Outbreak of Enterobacter cloacae related to
understaffing, overcrowding, and poor hygiene practices. Infect Control Hosp Epidemiol
1999; 20:598.
59. Sherman, MP, Goetzman, BW, Ahlfors, CE, Wennberg, RP. Tracheal asiration and its clinical
correlates in the diagnosis of congenital pneumonia. Pediatrics 1980; 65:258.
60. Brook, I, Martin, WJ, Finegold, SM. Bacteriology of tracheal aspirates in intubated newborn.
Chest 1980; 78:875.
61. Jolley, AE. The value of surveillance cultures on neonatal intensive care units. J Hosp Infect
1993; 25:153.
62. Lau, YL, Hey, E. Sensitivity and specificity of daily tracheal aspirate cultures in predicting
organisms causing bacteremia in ventilated neonates. Pediatr Infect Dis J 1991; 10:290.
63. Booth, GR, Al-Hosni, M, Ali, A, Keenan, WJ. The utility of tracheal aspirate cultures in the
immediate neonatal period. J Perinatol 2009; 29:493.
64. Haney, PJ, Bohlman, M, Sun, CC. Radiographic findings in neonatal pneumonia. AJR Am J
Roentgenol 1984; 143:23.
65. Cleveland, RH. A radiologic update on medical diseases of the newborn chest. Pediatr Radiol
1995; 25:631.
66. Hemming, VG, McCloskey, DW, Hill, HR. Pneumonia in the neonate associated with group B
streptococcal septicemia. Am J Dis Child 1976; 130:1231.
67. Speer, M, Rosan, RC, Rudolph, AJ. Hemophilus influenzae infection in the neonate mimicking
respiratory distress syndrome. J Pediatr 1978; 93:295.
68. Bortolussi, R, Thompson, TR, Ferrieri, P. Early-onset pneumococcal sepsis in newborn
infants. Pediatrics 1977; 60:352.
69. Edwards, MS. Antibacterial therapy in pregnancy and neonates. Clin Perinatol 1997; 24:251.
70. Gustaferro, CA, Steckelberg, JM. Cephalosporin antimicrobial agents and related
compounds. Mayo Clin Proc 1991; 66:1064.
71. Perl, TM. The threat of vancomycin resistance. Am J Med 1999; 106:26S.
72. American Academy of Pediatrics. Herpes simplex. In: Red Book: 2009 Report of the
Committee on Infectious Diseases, 28th ed, Pickering, LK (Ed), American Academy of
Pediatrics, Elk Grove Village, IL, 2009. p.363.
73. Randolph, AG, Wang, EE. Ribavirin for respiratory syncytial virus infection of the lower
respiratory tract. Cochrane Database Syst Rev 2000; :CD000181.
GRAPHICS


Common organisms associated with neonatal pneumonia according to route of
acquisition
Transplacental
Rubella
Cytomegalovirus
Herpes simplex virus
Adenovirus
Mumps virus
Toxoplasma gondii
Mycobacterium tuberculosis
Treponema pallidum
Listeria monocytogenes
At delivery
Group B streptococci
Escherichia coli
Staphylococcus aureus
Klebsiella sp
Other streptococci
Haemophilus influenzae (nontypable)
Candida sp
Chlamydia tachomatis
Ureaplasma urealyticum
Amniotic fluid
Cytomegalovirus
Herpes simplex virus
Enteroviruses
Genital mycoplasma
Listeria monocytogenes
Chlamydia trachomatis
Mycobacterium tuberculosis
Escherichia coli
Haemophilus influenzae (nontypable)
Ureaplasma urealyticum
Nosocomial
Staphylococcus aureus
Staphylococcus epidermidis
Klebsiella sp
Enterobacter
Pseudomonas
Bacillus cereus
Citrobacter diversus
Influenza virus
Respiratory synctial virus
Enteroviruses
Herpes virus
Candida sp
Aspergillus sp

2010 UpToDate, Inc. All rights reserved. | Subscription and License Agreement | Support Tag:
[ecapp0604p.utd.com-168.226.8.237-05254838C0-2579]
Licensed to: UpToDate Guest Pass - paola bruzzone | Your UpToDate trial will expire in 16
day(s). Click here to subscribe.

Noninfectious causes of respiratory distress
Anatomic/development defects
Primary pulmonary hypoplasia
Cystic adenomatoid malformation
Tracheoesophageal fistula
Diaphragmatic hernia
Congenital heart disease
Choanal atresia
Tracheal web
Laryngotracheomalacia
External compression of the trachea (eg, goiter)
Central nervous system malformation
Hydrocephalus
Genetic (eg, immotile cilia syndrome, surfactant protein B
deficiency, urea cycle defect)
Physiologic/pathologic disorders
Transient tachypnea of the
newborn
Respiratory distress syndrome
Meconium aspiration
pneumonia
Pulmonary hemorrhage
Pulmonary edema
Pneumothorax
Hydrothorax/chylothorax
Aspiration pneumonia
Hypoglycemia
Metabolic acidosis
Respiratory alkalosis
Central nervous system injury

Neonatal Pneumonia

Uploaded by

Document Information

Original Description:

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Neonatal Pneumonia

Uploaded by

Copyright:

Available Formats

Official reprint from UpToDate

You might also like