Pneumonia is an inflammatory pulmonary process that may originate in the lung or be a focal complication of a contiguous or systemic inflammatory process. Abnormalities of airway patency as well as alveolar ventilation and perfusion occur frequently due to various mechanisms. These derangements often significantly alter gas exchange and dependent cellular metabolism in the many tissues and organs that determine survival and contribute to quality of life.
Such pathologic problems, superimposed on the underlying difficulties associated with the transition from intrauterine to extrauterine life, pose critical challenges to the immature human organism. Recognition, prevention, and treatment of these problems are major factors in the care of high-risk newborn infants.
This article focuses on pneumonia that presents within the first 24 hours after birth. Although pneumonia is an important cause of morbidity and mortality among ne wborn infants, it remains a difficult disease to identify promptly and treat. [1, 2, 3, 4] (See Treatment and Management, as well as Medication.)
Clinical manifestations are often nonspecific (see Clinical Presentation).
Neonatal pneumonia shares respiratory and hemodynamic signs with a host of noninflammatory processes.  (See Diagnosis.)
Radiographic and laboratory findings have limited predictive value. (See Workup.)
Therapy in infants with neonatal pneumonia is multifaceted and includes both antimicrobial therapy and respiratory support. The goals of therapy are to eradicate infection and provide adequate support of gas exchange to ensure the survival and eventual well being of the infant (see Treatment and Management).
Pneumonia that becomes clinically evident within 24 hours of birth may originate at 3 different times. The 3 categories of congenital pneumonia are as follows:
True congenital pneumonia
True congenital pneumonia is already established at birth. It may become established long before birth or relatively shortly before birth. Transmission of congenital pneumonia usually occurs via 1 of 3 routes:
If the mother has a bloodstream infection, the microorganism can readily cross the few cell layers that separate the maternal from the fetal circulation at the villous pools of the placenta. The mother may be febrile or have other signs of infection, depending on the integrity of her host defenses, the responsible organism, and other considerations.
Transient bacteremia following daily activities, such as brushing teeth, defecating, and other potential disruptions of colonized mucoepithelial surfaces, is a well known phenomenon and may result in hematogenous transmission without significant maternal illness. However, the likelihood of hematogenous transmission is increased if the mother has continuous bloodstream infection with a relatively large quantity of microorganisms. In this case, the mother is more likely to have suggestive signs and symptoms.
Because host defenses are limited in fetuses, dissemination and illness may result. The fetus is likely to have systemic disease.
Ascending infection from the birth canal and aspiration of infected or inflamed amniotic fluid have significant common features. Infection of amniotic fluid often involves ascending pathogens from the birth canal but may result from hematogenous seeding or direct introduction during pelvic examination, amniocentesis, placement of intrauterine catheters, or other invasive procedures. Ascension may occur with or without ruptured amniotic membranes.
Most bacterial infections produce clinical signs of infection in the mother, but infections may not be evident if the membranes rupture shortly after inoculation, similar to drainage of an abscess. Some nonbacterial organisms, such as Ureaplasma species (U urealyticum or Uparvum), may be present in the amniotic cavity for long periods yet cause minimal symptoms in the mother.
If the fetus aspirates infected fluid prior to delivery, organisms that reach the distal airways or alveoli may need to cross only 2 cell layers (alveolar epithelium and capillary endothelium) to enter the bloodstream. Typically, these infants present with more pulmonary than systemic signs, but this is not always the case.
Intrapartum pneumonia is acquired during passage through the birth canal. It may be acquired via hematogenous or ascending transmission, from aspiration of infected or contaminated maternal fluids, or from mechanical or ischemic disruption of a mucosal surface that has been freshly colonized with a maternal organism of appropriate invasive potential and virulence.
Postnatal pneumonia in the first 24 hours of life originates after the infant has left the birth canal. It may result from some of the same processes described above, but infection occurs after the birth process. Colonization of a mucoepithelial surface with an appropriate pathogen from a maternal or environmental source and subsequent disruption allows the organism to enter the bloodstream, lymphatics, or deep parenchymal structures.
The frequent use of broad-spectrum antibiotics in many obstetrical services and neonatal intensive care units (NICUs) often results in predisposition of an infant to colonization by resistant organisms of unusual pathogenicity. Invasive therapies typically required in these infants often allow microbes accelerated entry into deep structures that ordinarily are not easily accessible.
Enteral feedings may result in aspiration events of significant inflammatory potential. Indwelling feeding tubes may further predispose infants to gastroesophageal reflux and other aspiration events.
In neonatal pneumonia, pulmonary and extrapulmonary injuries are caused directly and indirectly by invading microorganisms or foreign material and by poorly targeted or inappropriate responses by the host defense system that may damage healthy host tissues as badly or worse than the invading agent. Direct injury by the invading agent usually results from synthesis and secretion of microbial enzymes, proteins, toxic lipids, and toxins that disrupt host cell membranes, metabolic machinery, and the extracellular matrix that usually inhibits microbial migration. [6, 7]
Indirect injury is mediated by structural or secreted molecules, such as endotoxin, leukocidin, and toxic shock syndrome toxin-1, which may alter local vasomotor tone and integrity, change the characteristics of the tissue perfusate, and generally interfere with the delivery of oxygen and nutrients and removal of waste products from local tissues.
The activated inflammatory response often results in targeted migration of phagocytes, with the release of toxic substances from granules and other microbicidal packages and the initiation of poorly regulated cascades (eg, complement, coagulation, cytokines). These cascades may directly injure host tissues and adversely alter endothelial and epithelial integrity, vasomotor tone, intravascular hemostasis, and the activation state of fixed and migratory phagocytes at the inflammatory focus. The role of apoptosis (noninflammatory programmed cell death) in pneumonia is poorly understood.
On a macroscopic level, the invading agents and the host defenses both tend to increase airway smooth muscle tone and resistance, mucous secretion, and the presence of inflammatory cells and debris in these secretions. These materials may further increase airway resistance and obstruct the airways, partially or totally, causing airtrapping, atelectasis, and ventilatory dead space. In addition, disruption of endothelial and alveolar epithelial integrity may allow surfactant to be inactivated by proteinaceous exudate, a process that may be exacerbated further by the direct effects of meconium or pathogenic microorganisms.
In the end, conducting airways offer much more resistance and may become obstructed, alveoli may be atelectatic or hyperexpanded, alveolar perfusion may be markedly altered, and multiple tissues and cell populations in the lung and elsewhere sustain injury that increases the basal requirements for oxygen uptake and excretory gas removal at a time when the lungs are less able to accomplish these tasks.
Alveolar diffusion barriers may increase, intrapulmonary shunts may worsen, and ventilation-perfusion mismatch may further impair gas exchange despite endogenous homeostatic attempts to improve matching by regional airway and vascular constriction or dilatation. Because the myocardium has to work harder to overcome the alterations in pulmonary vascular resistance that accompany the above changes of pneumonia, the lungs may be less able to add oxygen and remove carbon dioxide from mixed venous blood for delivery to end organs. The spread of infection or inflammatory response, either systemically or to other focal sites, further exacerbates the situation.
Neonatal pneumonia may be infectious or noninfectious. Organisms responsible for infectious pneumonia typically mirror those responsible for early-onset neonatal sepsis. This is not surprising, in view of the role that maternal genitourinary and gastrointestinal tract flora play in both processes.
Group B Streptococcus (GBS) was the most common bacterial isolate in most locales from the late 1960s to the late 1990s, when the impact of intrapartum chemoprophylaxis in reducing neonatal and maternal infection by this organism became evident. Despite the decreased frequency, GBS remains a common isolate in early-onset (aged < 3 d) infections in term and near-term infants. Since that time, Escherichia coli has become the most common bacterial isolate among very low birth weight infants (≤1500 g).  Other prominent bacterial organisms include the following:
Nontypable Haemophilus influenzae
Other gram-negative bacilli
Occasionally, Staphylococcus aureus
Rarely, Mycoplasma pneumoniae 
Among nonbacterial potential pathogens, U urealyticum and U parvum have been frequently recovered from endotracheal aspirates shortly after birth in very low birth weight infants and have been variably associated with various adverse pulmonary outcomes, including bronchopulmonary dysplasia (BPD). [10, 11, 12, 13, 14] Whether this organism is causal or simply a marker of increased risk is unclear.
Numerous comparative therapeutic trials have suggested that BPD prevention offers no or limited benefit among certain subgroups. These organisms have also been recovered from normally sterile sites (eg, blood, cerebrospinal fluid [CSF], lung tissue) in critically ill infants in whom antimicrobial treatment appeared to be warranted. Whether the improvement was due to or despite such treatment remains controversial.
Agents of chronic congenital infection, such as cytomegalovirus, Treponema pallidum, Toxoplasma gondii, rubella, and others, may cause pneumonia in the first 24 hours of life. Clinical presentation usually involves other organ systems as well. [15, 16]
Chlamydia organisms presumably are transmitted at birth during passage through an infected birth canal, although most infants are asymptomatic during the first 24 hours and develop pneumonia only after the first 2 weeks of life.
Few case reports have identified vertical transmission of Neisseria gonorrhoeae causing congenital pneumonia. However, in a recent study, the blood and sputum cultures were negative but the cells of N gonorrhea were obtained in gastric aspirate culture. The chest radiograph was consistent with fine reticulogranular infiltration, confirming pneumonia. 
Infections with Streptococcus pneumonia (Pneumococcus) are infrequent in the neonatal period but are associated with high morbidity and mortality rates. In the neonatal period, pneumococcal infections can present in the form of pneumonia, sepsis, or meningitis with early or late onset. The transmission of the organism is not clear but is suspected to be either by vertical transmission from vaginal colonization of Pneumococcus or horizontal due to local infections or infections by nonvaccine serogroups. 
Respiratory viral pathogens such as respiratory syncytial virus, influenza virus, adenovirus, and others may be transmitted vertically or shortly after birth by contact with infected family members or caregivers. However, infection by immediate postnatal transmission of these organisms rarely becomes apparent during the first 24 hours.
Congenital tuberculosis is rare but fatal cause of congenital pneumonia if left untreated. An untreated pregnant woman with tuberculosis can spread infection to a fetus by hematogenous spread through the umbilical cord or by aspiration or ingestion of amniotic fluid. Signs and symptoms of congenital tuberculosis may be nonspecific, which may preclude early diagnosis and treatment. [19, 20]
Congenital candidiasis can lead to pneumonia and respiratory distress within 24 hours of life. In addition, it is characterized by diffuse erythematous papules. 
Pneumonia occurs frequently in newborn infants, although reported rates vary considerably depending on the diagnostic criteria used and the characteristics of the population under study. Most reports cite frequencies in the range of 5-50 per 1000 live births, with higher rates in the settings of maternal chorioamnionitis, prematurity, and meconium in the amniotic fluid. Many cases are likely unreported or undetected; thus, the cited frequency is almost certainly a low estimate.
Determination of mortality rates among infants with congenital pneumonia is complicated by variations in diagnostic criteria and the thoroughness with which this condition is sought. Among infants with congenital pneumonia associated with proven blood-borne infection, mortality is in the range of 5-10%, with rates as high as 30% in infants with very low birth weight. Pneumonia is a contributing factor in 10-25% of all deaths that occur in neonates younger than 30 days.
Continued growth and development of pulmonary and other tissues offers good prospects for long-term survival and progressive improvement in most infants who survive congenital pneumonia. Nevertheless, although quantitation of risk is difficult and is strongly influenced by gestational age, congenital anomalies, and coexisting cardiovascular disease, there is a consensus that congenital pneumonia increases the following:
Chronic lung disease
Prolonged need for respiratory support
Childhood otitis media
Reactive airway disease
Severity of subsequent early childhood respiratory infections
Complications attendant to these conditions
Significant predictors of mortality in ventilated patients include the following  :
Education of parents whose infant has had congenital pneumonia is principally directed toward subsequent care. Counsel parents regarding the need to prevent exposure of infants to tobacco smoke. Educate parents regarding the benefit infants may receive from pneumococcal immunization and annual influenza immunization. Discuss potential benefits and costs of respiratory syncytial virus immune globulin.
As part of anticipatory primary care, educate parents regarding later infectious exposures in daycare centers, schools, and similar settings and the importance of hand washing. Emphasize careful longitudinal surveillance for long-term problems with growth, development, otitis, reactive airway disease, and other complications.
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Muhammad Aslam, MD Associate Professor of Pediatrics, University of California, Irvine, School of Medicine; Neonatologist, Division of Newborn Medicine, Department of Pediatrics, UC Irvine Medical Center
Muhammad Aslam, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
Brian S Carter, MD, FAAP Professor of Pediatrics, University of Missouri-Kansas City School of Medicine; Attending Physician, Division of Neonatology, Children’s Mercy Hospital and Clinics; Faculty, Children’s Mercy Bioethics Center
Brian S Carter, MD, FAAP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Pediatric Society, American Society for Bioethics and Humanities, American Society of Law, Medicine & Ethics, Society for Pediatric Research, National Hospice and Palliative Care Organization
Disclosure: Nothing to disclose.
Ted Rosenkrantz, MD Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine
Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, Eastern Society for Pediatric Research, American Medical Association, Connecticut State Medical Society, Society for Pediatric Research
Disclosure: Nothing to disclose.
Mariam L Abdul-Latif, MD Neonatal-Perinatal Medicine Fellow, Department of Pediatrics, University of California, Irvine, School of Medicine
Disclosure: Nothing to disclose.
Roger G Faix, MD Professor, Department of Pediatrics (Neonatology), University of Utah School of Medicine
Roger G Faix, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, American Society for Microbiology, National Perinatal Association, Society for Pediatric Research, and Utah Medical Association
Disclosure: Nothing to disclose.
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