Neonatal Sepsis

Neonatal Sepsis

No Results

No Results


Neonatal sepsis may be categorized as early-onset or late-onset. Of newborns with early-onset sepsis, 85% present within 24 hours, 5% present at 24-48 hours, and a smaller percentage present within 48-72 hours. Onset is most rapid in premature neonates.

Early-onset sepsis is associated with acquisition of microorganisms from the mother. Transplacental infection or an ascending infection from the cervix may be caused by organisms that colonize the mother’s genitourinary (GU) tract; the neonate acquires the microorganisms as it passes through the colonized birth canal at delivery. The microorganisms most commonly associated with early-onset infection include the following [1] :

Group B Streptococcus (GBS)

Escherichia coli

Coagulase-negative Staphylococcus

Haemophilus influenzae

Listeria monocytogenes

Trends in the epidemiology of early-onset sepsis show a decreasing incidence of GBS disease. This can be attributed to the implementation of a prenatal screening and treatment protocol for GBS.

In a 2009 study involving 4696 women, prenatal cultures showed a GBS colonization rate of 24.5%, with a positive culture rate of 18.8% at the time of labor. As many as 10% of prenatally culture-negative women were found to have positive cultures at the time of labor. With intrapartum antibiotic prophylaxis rates of 93.3%, 0.36 of 1000 infants developed early-onset GBS disease. [2, 3]

Late-onset sepsis occurs at 4-90 days of life and is acquired from the caregiving environment. Organisms that have been implicated in causing late-onset sepsis include the following:

Coagulase-negative Staphylococcus

Staphylococcus aureus

E coli









Trends in late-onset sepsis show an increase in coagulase-negative streptococcal sepsis; most of these isolates are susceptible to first-generation cephalosporins. [2] The infant’s skin, respiratory tract, conjunctivae, gastrointestinal (GI) tract, and umbilicus may become colonized from the environment, and such colonization to the possibility of late-onset sepsis from invasive microorganisms. Vectors for such colonization may include vascular or urinary catheters, other indwelling lines, or contact with caregivers who have bacterial colonization.

Pneumonia is more common in early-onset sepsis, whereas meningitis and bacteremia are more common in late-onset sepsis. Premature and ill infants are more susceptible to sepsis and subtle nonspecific initial presentations; considerable vigilance is therefore required in these patients so that sepsis can be effectively identified and treated.

When neonatal sepsis is suspected, treatment should be initiated immediately because of the neonate’s relative immunosuppression. Begin antibiotics as soon as diagnostic tests are performed (see Treatment).

For patient education information, see Sepsis (Blood Infection).

The infectious agents associated with neonatal sepsis have changed since the mid-20th century. During the 1950s, S aureus and E coli were the most common bacterial pathogens among neonates in the United States. Over the ensuing decades, GBS replaced S aureus as the most common gram-positive organism that caused early-onset sepsis.

During the 1990s, GBS and E coli continued to be associated with neonatal infection; however, coagulase-negative Staphylococcus epidermidis is now more frequently observed. Additional organisms, such as L monocytogenes, Chlamydia pneumoniae, H influenzae, Enterobacter aerogenes, and species of Bacteroides and Clostridium have also been identified in neonatal sepsis.

Meningoencephalitis and neonatal sepsis can also be caused by infection with adenovirus, enterovirus, or coxsackievirus. Additionally, sexually transmitted diseases (eg, gonorrhea, syphilis, herpes simplex virus [HSV] infection, cytomegalovirus [CMV] infection, hepatitis, human immunodeficiency virus [HIV] infection, rubella, toxoplasmosis, trichomoniasis, and candidiasis) have all been implicated in neonatal infection.

Bacterial organisms with increased antibiotic resistance have also emerged and have further complicated the management of neonatal sepsis. [4] The colonization patterns in nurseries and personnel are reflected in the organisms currently associated with nosocomial infection. In neonatal intensive care units (NICUs), infants with lower birth weight and infants who are less mature have an increased susceptibility to these organisms.

S epidermidis, a coagulase-negative Staphylococcus, is increasingly seen as a cause of nosocomial or late-onset sepsis, especially in the premature infant, in whom it is considered the leading cause of late-onset infections. Its prevalence is likely related to several intrinsic properties of the organism that allow it to readily adhere to the plastic mediums found in intravascular catheters and intraventricular shunts.

The bacterial capsule polysaccharide adheres well to the plastic polymers of the catheters. Also, proteins found in the organism (AtlE and SSP-1) enhance attachment to the surface of the catheter. The adherence creates a capsule between microbe and catheter, preventing C3 deposition and phagocytosis.

Biofilms are formed on indwelling catheters by the aggregation of organisms that have multiplied under the protection provided by the adherence to the catheter. Slimes are produced at the site from the extracellular material formed by the organism, which provides a barrier to host defense as well as to antibiotic action, making coagulase-negative staphylococcal bloodstream infection (BSI) more difficult to treat. The toxins formed by this organism have also been associated with necrotizing enterocolitis.

In addition to being a cause of neonatal sepsis, coagulase-negative Staphylococcus is ubiquitous as part of the normal skin flora. Consequently, it is a frequent contaminant of blood and cerebrospinal fluid (CSF) cultures. When a culture grows this organism , the clinical setting, colony counts, and the presence of polymorphonuclear neutrophils (PMNs) on Gram staining of the submitted specimen often help differentiate true infection and positive culture from a false-positive or contaminated specimen.

In addition to the specific microbial factors mentioned above, numerous host factors predispose the newborn to sepsis. [5] These factors are especially prominent in the premature  infant and involve all levels of host defense, including cellular immunity, humoral immunity, and barrier function. Immature immune defenses, and environmental and maternal factors contribute to the risk neonatal sepsis, morbidity, and mortality, particularly in preterm and/or very low birthweight (VLBW) infants. [5, 6]  There may also be a genetic association. [5]

PMNs are vital for effective killing of bacteria. However, neonatal PMNs are deficient in chemotaxis and killing capacity. Decreased adherence to the endothelial lining of blood vessels reduces their ability to marginate and leave the intravascular space to migrate into the tissues. Once in the tissues, they may fail to degranulate in response to chemotactic factors.

Furthermore, neonatal PMNs are less deformable and thus are less able to move through the extracellular matrix of tissues to reach the site of inflammation and infection. The limited capacity of neonatal PMNs for phagocytosis and killing of bacteria is further impaired when the infant is clinically ill. Finally, neutrophil reserves are easily depleted because of the diminished response of the bone marrow, especially in the premature infant.

Neonatal monocyte concentrations are at adult levels; however, macrophage chemotaxis is impaired and continues to exhibit decreased function into early childhood. The absolute numbers of macrophages are decreased in the lungs and are likely decreased in the liver and spleen as well. The chemotactic and bactericidal activity and the antigen presentation by these cells are also not fully competent at birth. Cytokine production by macrophages is decreased, which may be associated with a corresponding decrease in T-cell production.

Although T cells are found in early gestation in fetal circulation and increase in number from birth to about age 6 months, these cells represent an immature population. These naive cells do not proliferate as readily as adult T cells do when activated, and they do not effectively produce the cytokines that assist with B-cell stimulation and differentiation and granulocyte/monocyte proliferation.

Formation of antigen-specific memory function after primary infection is delayed, and the cytotoxic function of neonatal T cells is 50-100% as effective as that of adult T cells. At birth, neonates are deficient in memory T cells. As the neonate is exposed to antigenic stimuli, the number of these memory T cells increases.

Natural killer (NK) cells are found in small numbers in the peripheral blood of neonates. These cells are also functionally immature in that they produce far lower levels of interferon gamma (IFN-γ) upon primary stimulation than adult NK cells do. This combination of findings may contribute to the severity of HSV infections in the neonatal period.

The fetus has some preformed immunoglobulin, which is primarily acquired through nonspecific placental transfer from the mother. Most of this transfer occurs in late gestation, so that lower levels are found with increasing prematurity. The neonate’s ability to generate immunoglobulin in response to antigenic stimulation is intact; however, the magnitude of the response is initially decreased, rapidly rising with increasing postnatal age.

The neonate is also capable of synthesizing immunoglobulin M (IgM) in utero at 10 weeks’ gestation; however, IgM levels are generally low at birth, unless the infant was exposed to an infectious agent during the pregnancy, which would have stimulated increased IgM production.

Immunoglobulin G (IgG) and immunoglobulin E (IgE) may be synthesized in utero. Most of the IgG is acquired from the mother during late gestation. The neonate may receive immunoglobulin A (IgA) from breastfeeding but does not secrete IgA until 2-5 weeks after birth. Response to bacterial polysaccharide antigen is diminished and remains so during the first 2 years of life.

Complement protein production can be detected as early as 6 weeks’ gestation; however, the concentration of the various components of the complement system varies widely from one neonate to another. Although some infants have had complement levels comparable to those in adults, deficiencies appear to be greater in the alternative pathway than in the classic pathway.

The terminal cytotoxic components of the complement cascade that lead to killing of organisms, especially gram-negative bacteria, are deficient. This deficiency is more marked in preterm infants. Mature complement activity is not reached until infants are aged 6-10 months. Neonatal sera have reduced opsonic efficiency against GBS, E coli, and Streptococcus pneumoniae because of decreased levels of fibronectin, a serum protein that assists with neutrophil adherence and has opsonic properties.

The physical and chemical barriers to infection in the human body are present in the newborn but are functionally deficient. Skin and mucous membranes are broken down easily in the premature infant. Neonates who are ill, premature, or both are at additional risk because of the invasive procedures that breach their physical barriers to infection.

Because of the interdependence of the immune response, these individual deficiencies of the various components of immune activity in the neonate conspire to create a hazardous situation for the neonate exposed to infectious threats.

In overwhelming sepsis, there may be an initial early phase characterized by pulmonary hypertension, decreased cardiac output, and hypoxemia. These cardiopulmonary disturbances may be due to the activity of granulocyte-derived biochemical mediators, such as hydroxyl radicals and thromboxane B2 (an arachidonic acid metabolite).

These biochemical agents have vasoconstrictive actions that result in pulmonary hypertension when they are released in pulmonary tissue. A toxin derived from the polysaccharide capsule of type III Streptococcus has also been shown to cause pulmonary hypertension.

The intestines can be colonized by organisms in utero or at delivery through swallowing of infected amniotic fluid. The immunologic defenses of the GI tract are not mature, especially in the preterm infant. Lymphocytes proliferate in the intestines in response to mitogen stimulation; however, this proliferation is not fully effective in responding to a microorganism, because antibody response and cytokine formation are immature until approximately 46 weeks.

Necrotizing enterocolitis has been associated with the presence of a number of species of bacteria in the immature intestine. Overgrowth of these organisms in the neonatal lumen is a component of the multifactorial pathophysiology of necrotizing enterocolitis.


Ventriculitis is the initiating event in meningitis, with inflammation of the ventricular surface. Exudative material usually appears at the choroid plexus and is external to the plexus. Ependymitis then occurs, with disruption of the ventricular lining and projections of glial tufts into the ventricular lumen. Glial bridges may develop by these tufts and cause obstruction, particularly at the aqueduct of Sylvius.

The lateral ventricles may become multiloculated, a process that is similar to formation of abscesses. Multiloculated ventricles can isolate organisms in an area, making treatment more difficult.

Meningitis is likely to arise at the choroid plexus and extend via the ventricles through aqueducts and into the subarachnoid space to affect the cerebral and cerebellar surfaces. The high glycogen content in the neonatal choroid plexus provides an excellent medium for the bacteria. When meningitis develops from ventriculitis, effective treatment is complicated because adequate antibiotic levels in the cerebral ventricles are difficult to achieve. When ventricular obstruction is present, it causes additional problems.


Arachnoiditis is the next phase of the process and is the hallmark of meningitis. The arachnoid is infiltrated by inflammatory cells producing an exudate that is thick over the base of the brain and more uniform over the rest of the brain. Early in the infection, the exudate primarily contains PMNs, bacteria, and macrophages. It is prominent around the blood vessels and extends into the brain parenchyma.

In the second and third weeks of infection, the proportion of PMNs decreases; the dominant cells are histiocytes, macrophages, and some lymphocytes and plasma cells. Exudate infiltration of cranial roots 3-8 occurs.

After this period, the exudate decreases. Thick strands of collagen form, and arachnoid fibrosis occurs, which is responsible for obstruction. Hydrocephalus results. Early-onset GBS meningitis is characterized by much less arachnoiditis than late-onset GBS meningitis is.


Vasculitis extends the inflammation of the arachnoid and ventricles to the blood vessels surrounding the brain. Occlusion of the arteries rarely occurs; however, venous involvement is more severe. Phlebitis may be accompanied by thrombosis and complete occlusion. Multiple fibrin thrombi are especially associated with hemorrhagic infarction. This vascular involvement is apparent within the first days of meningitis and becomes more prominent during the second and third weeks.

Cerebral edema

Cerebral edema may occur during the acute state of meningitis and may be severe enough to diminish the ventricular lumen substantially. The cause is unknown but is likely to be related to vasculitis and the increased permeability of blood vessels. It may also be related to cytotoxins of microbial origin. Herniation of edematous supratentorial structures does not generally occur in neonates, because of the cranium’s distensibility.


Infarction is a prominent and serious feature of neonatal meningitis, occurring in 30% of infants who die. Lesions occur because of multiple venous occlusions, which are frequently hemorrhagic. The loci of infarcts are most often in the cerebral cortex and underlying white matter but may also be subependymal within the deep white matter. Neuronal loss occurs, especially in the cerebral cortex, and periventricular leukomalacia may subsequently appear in areas of neuronal cell death.

The microorganisms most commonly associated with early-onset neonatal sepsis include the following [1] :


E coli

Coagulase-negative Staphylococcus

H influenzae

L monocytogenes

Risk factors implicated in neonatal sepsis reflect the level stress and illness experienced by the fetus at delivery, as well as the hazardous uterine environment surrounding the fetus before delivery. The most common risk factors associated with early-onset neonatal sepsis are as follows:

Maternal GBS colonization (especially if untreated during labor)

Premature rupture of membranes (PROM)

Preterm rupture of membranes

Prolonged rupture of membranes


Maternal urinary tract infection


Other factors that are associated with or predispose to early-onset neonatal sepsis include the following [7, 8] :

Low Apgar score (< 6 at 1 or 5 minutes)

Maternal fever greater than 38°C

Maternal urinary tract infection (UTI)

Poor prenatal care

Poor maternal nutrition

Low socioeconomic status

African American mother

History of recurrent abortion

Maternal substance abuse

Low birth weight

Difficult delivery

Birth asphyxia

Meconium staining

Congenital anomalies

Organisms that have been implicated in causing late-onset neonatal sepsis include the following:

Coagulase-negative staphylococci

S aureus

E coli









Late-onset sepsis is associated with the following risk factors [9] :


Central venous catheterization (duration >10 days)

Nasal cannula or continuous positive airway pressure (CPAP) use

H2 -receptor blocker or proton pump inhibitor (PPI) use

GI tract pathology

The principal pathogens in neonatal meningitis are GBS (36% of cases), E coli (31%), and Listeria species (5-10%). Other organisms that may cause meningitis include the following:

S pneumoniae

S aureus

S epidermidis

H influenzae

Pseudomonas species

Klebsiella species

Serratia species

Enterobacter species

Proteus species

The incidence of culture-proven sepsis in the United States is approximately 2 per 1000 live births. Of the 7-13% of neonates who are evaluated for neonatal sepsis, only 3-8% have culture-proven sepsis. This disparity arises from the cautious approach to management of neonatal sepsis.

Because early signs of sepsis in the newborn are nonspecific, diagnostic studies are often ordered and treatment initiated in neonates before the presence of sepsis has been proved. Moreover, because the American Academy of Pediatrics (AAP), [10] the American Academy of Obstetrics and Gynecology (AAOG), and the Centers for Disease Control and Prevention (CDC) [11] all have recommended sepsis screening or treatment for various risk factors related to GBS infections, many asymptomatic neonates now undergo evaluation.

Because mortality from untreated sepsis can be as high as 50%, most clinicians believe that the hazard of untreated sepsis is too great to allow them to wait for confirmation in the form of positive culture results. Therefore, most clinicians initiate treatment while awaiting culture results.

The implementation of a prenatal screening and treatment protocol for GBS has resulted in a decreasing incidence of GBS sepsis. This has changed the epidemiology of early-onset sepsis (see the image below).

Black infants have an increased incidence of GBS disease and late-onset sepsis. This is observed even after the risk factors of low birth weight and decreased maternal age have been controlled for. This may be in part due to higher carriage rates of GBS among African American women, but this does not explain all of the variation. [8] In all races, the incidence of bacterial sepsis and meningitis, especially with gram-negative enteric bacilli, is higher in males than in females.

Premature infants have an increased incidence of sepsis. The incidence of sepsis is significantly higher in infants with a birth weight of less than 1000 g (26 per 1000 live births) than in infants with a birth weight of 1000-2000 g (8-9 per 1000 live births). The risk of death or meningitis from sepsis is higher in infants with low birth weight than in full-term neonates.

With early diagnosis and treatment, term infants are not likely to experience long-term health problems associated with neonatal sepsis; however, if early signs or risk factors are missed, mortality increases. Residual neurologic damage occurs in 15-30% of neonates with septic meningitis.

Mortality from neonatal sepsis may be as high as 50% for infants who are not treated. Infection is a major cause of fatality during the first month of life, contributing to 13-15% of all neonatal deaths. Low birth weight and gram-negative infection are associated with adverse outcomes. [12] Neonatal meningitis occurs in 2-4 cases per 10,000 live births and contributes significantly to mortality from neonatal sepsis; it is responsible for 4% of all neonatal deaths.

In preterm infants who have had sepsis, impaired neurodevelopment is a concern. [13] Proinflammatory molecules may negatively affect brain development in this patient population. In a large study of about 6000 premature infants who weighed less than 1000 g at birth, preterm infants with sepsis who did not have meningitis had higher rates of cognitive deficits, cerebral palsy, and other neurodevelopmental disabilities than infants who did not have sepsis. [14, 15]

Infants with meningitis may acquire hydrocephalus or periventricular leukomalacia. They may also have complications associated with the use of aminoglycosides, such as hearing loss or nephrotoxicity.

Klinger G, Levy I, Sirota L, et al. Epidemiology and risk factors for early onset sepsis among very-low-birthweight infants. Am J Obstet Gynecol. 2009 Jul. 201(1):38.e1-6. [Medline].

van den Hoogen A, Gerards LJ, Verboon-Maciolek MA, Fleer A, Krediet TG. Long-term trends in the epidemiology of neonatal sepsis and antibiotic susceptibility of causative agents. Neonatology. 2010. 97(1):22-8. [Medline].

Lin FY, Weisman LE, Azimi P, et al. Assessment of Intrapartum Antibiotic Prophylaxis for the Prevention of Early-onset Group B Streptococcal Disease. Pediatr Infect Dis J. 2011 Sep. 30(9):759-763. [Medline]. [Full Text].

Morales WJ, Dickey SS, Bornick P, Lim DV. Change in antibiotic resistance of group B streptococcus: impact on intrapartum management. Am J Obstet Gynecol. 1999 Aug. 181(2):310-4. [Medline].

Srinivasan L, Kirpalani H, Cotten CM. Elucidating the role of genomics in neonatal sepsis. Semin Perinatol. 2015 Dec. 39 (8):611-6. [Medline].

Groer MW, Gregory KE, Louis-Jacques A, Thibeau S, Walker WA. The very low birth weight infant microbiome and childhood health. Birth Defects Res C Embryo Today. 2015 Dec 10. [Medline].

Arnon S, Litmanovitz I. Diagnostic tests in neonatal sepsis. Curr Opin Infect Dis. 2008 Jun. 21(3):223-7. [Medline].

Simonsen KA, Anderson-Berry AL, Delair SF, Davies HD. Early-onset neonatal sepsis. Clin Microbiol Rev. 2014 Jan. 27(1):21-47. [Medline].

Graham PL, Begg MD, Larson E. Risk factors for late onset gram-negative sepsis in low birth weight infants hospitalized in the neonatal intensive care unit. Pediatr Infect Dis J. 2006 Feb. 25(2):113-7. [Medline].

[Guideline] American Academy of Pediatrics. Red Book 2003. 26th ed. 2003. 117-123, 237-43, 561-73,584-91.

[Guideline] Schrag S, Gorwitz R, Fultz-Butts K, Schuchat A. Prevention of perinatal group B streptococcal disease. Revised guidelines from CDC. MMWR Recomm Rep. 2002 Aug 16. 51(RR-11):1-22. [Medline].

Kermorvant-Duchemin E, Laborie S, Rabilloud M, Lapillonne A, Claris O. Outcome and prognostic factors in neonates with septic shock. Pediatr Crit Care Med. 2008 Mar. 9(2):186-91. [Medline].

Adams-Chapman I, Stoll BJ. Neonatal infection and long-term neurodevelopmental outcome in the preterm infant. Curr Opin Infect Dis. 2006 Jun. 19(3):290-7. [Medline].

Volpe JJ. Postnatal sepsis, necrotizing entercolitis, and the critical role of systemic inflammation in white matter injury in premature infants. J Pediatr. 2008 Aug. 153(2):160-3. [Medline]. [Full Text].

Stoll BJ, Hansen NI, Adams-Chapman I, et al. Neurodevelopmental and growth impairment among extremely low-birth-weight infants with neonatal infection. JAMA. 2004 Nov 17. 292(19):2357-65. [Medline].

Seaward PG, Hannah ME, Myhr TL, et al. International multicenter term PROM study: evaluation of predictors of neonatal infection in infants born to patients with premature rupture of membranes at term. Premature Rupture of the Membranes. Am J Obstet Gynecol. 1998 Sep. 179(3 Pt 1):635-9. [Medline].

Short MA. Guide to a systematic physical assessment in the infant with suspected infection and/or sepsis. Adv Neonatal Care. 2004 Jun. 4(3):141-53; quiz 154-7. [Medline].

Delanghe JR, Speeckaert MM. Translational research and biomarkers in neonatal sepsis. Clin Chim Acta. 2015 Dec 7. 451 (Pt A):46-64. [Medline].

Chan KY, Lam HS, Cheung HM, et al. Rapid identification and differentiation of Gram-negative and Gram-positive bacterial bloodstream infections by quantitative polymerase chain reaction in preterm infants. Crit Care Med. 2009 Aug. 37(8):2441-7. [Medline].

Enomoto M, Morioka I, Morisawa T, Yokoyama N, Matsuo M. A novel diagnostic tool for detecting neonatal infections using multiplex polymerase chain reaction. Neonatology. 2009. 96(2):102-8. [Medline].

Sarkar S, Bhagat I, DeCristofaro JD. A study of the role of multiple site blood cultures in the evaluation of neonatal sepsis. J Perinatol. 2006 Jan 1. 26(1):18-22. [Medline].

Khashu M, Osiovich H, Henry D. Persistent bacteremia and severe thrombocytopenia caused by coagulase-negative Staphylococcus in a neonatal intensive care unit. Pediatrics. 2006 Feb. 117(2):340-8. [Medline].

Hawk M. C-reactive protein in neonatal sepsis. Neonatal Netw. 2008 Mar-Apr. 27(2):117-20. [Medline].

Ng PC, Lam HS. Diagnostic markers for neonatal sepsis. Curr Opin Pediatr. 2006 Apr. 18(2):125-31. [Medline].

Meem M, Modak JK, Mortuza R, Morshed M, Islam MS, Saha SK. Biomarkers for diagnosis of neonatal infections: A systematic analysis of their potential as a point-of-care diagnostics. J Glob Health. 2011 Dec. 1(2):201-9. [Medline].

Altunhan H, Annagür A, Örs R, Mehmetoglu I. Procalcitonin measurement at 24 hours of age may be helpful in the prompt diagnosis of early-onset neonatal sepsis. Int J Infect Dis. 2011 Dec. 15(12):e854-8. [Medline].

Ng PC, Li K, Leung TF. Early prediction of sepsis-induced disseminated intravascular coagulation with interleukin-10, interleukin-6, and RANTES in preterm infants. Clin Chem. 2006 Jun. 52(6):1181-9. [Medline].

Garges HP, Moody MA, Cotten CM. Neonatal meningitis: what is the correlation among cerebrospinal fluid cultures, blood cultures, and cerebrospinal fluid parameters?. Pediatrics. 2006 Apr. 117(4):1094-100. [Medline].

Davis KL, Shah SS, Frank G, Eppes SC. Why are young infants tested for herpes simplex virus?. Pediatr Emerg Care. 2008 Oct. 24(10):673-8. [Medline].

Tzialla C, Borghesi A, Pozzi M, Stronati M. Neonatal infections due to multi-resistant strains: Epidemiology, current treatment, emerging therapeutic approaches and prevention. Clin Chim Acta. 2015 Dec 7. 451 (Pt A):71-7. [Medline].

Shipp KD, Chiang T, Karasick S, Quick K, Nguyen ST, Cantey JB. Antibiotic stewardship challenges in a referral neonatal intensive care unit. Am J Perinatol. 2015 Dec 18. [Medline].

Zaidi AK, Tikmani SS, Warraich HJ, Darmstadt GL, Bhutta ZA, Sultana S, et al. Community-based Treatment of Serious Bacterial Infections in Newborns and Young Infants: A Randomized Controlled Trial Assessing Three Antibiotic Regimens. Pediatr Infect Dis J. 2012 Jul. 31(7):667-72. [Medline].

The INIS Collaborative Group. Treatment of neonatal sepsis with intravenous immune globulin. N Engl J Med. 2011 Sep 29. 365(13):1201-11. [Medline].

Manzoni P, Decembrino L, Stolfi I, et al. Lactoferrin and prevention of late-onset sepsis in the preterm neonate in the NICU. Early Hum Dev. 2010 Feb 5. [Medline].

Ann L Anderson-Berry, MD, PhD Associate Professor of Pediatrics, Section of Newborn Medicine, University of Nebraska Medical Center, Creighton University School of Medicine; Medical Director, NICU, Nebraska Medical Center

Ann L Anderson-Berry, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, Nebraska Medical Association, Society for Pediatric Research

Disclosure: Nothing to disclose.

Linda L Bellig, RN, MA, NNP-BC (Retired) Track Coordinator, Instructor, Neonatal Nurse Practitioner Program, Medical University of South Carolina College of Nursing

Disclosure: Nothing to disclose.

Bryan L Ohning, MD, PhD Medical Director of Neonatal Transport, Division of Neonatology, Children’s Hospital, Greenville Hospital System, University Medical Center; Professor of Clinical Pediatrics, University of South Carolina School of Medicine-Greenville

Bryan L Ohning, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, South Carolina Medical Association

Disclosure: Receive salary from Pediatrix Medical Group of SC for employment. for: Mednax.

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.

David A Clark, MD Chairman, Professor, Department of Pediatrics, Albany Medical College

David A Clark, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Pediatric Society, Christian Medical & Dental Society, Medical Society of the State of New York, New York Academy of Sciences, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Scott S MacGilvray, MD Clinical Professor, Department of Pediatrics, Division of Neonatology, The Brody School of Medicine at East Carolina University

Scott S MacGilvray, 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.

Neonatal Sepsis

Research & References of Neonatal Sepsis|A&C Accounting And Tax Services