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Neonatal Infections

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Author:    Patricia Hartley (RNC, MSN)


The basic function of the immune system is to protect the body from harm caused by infection invading microorganisms such as bacteria, viruses, fungi, protozoa and parasites. During gestation, the fetus grows and develops within the usually protective environment of its mother’s uterus. However, during the birth process and subsequently, the neonate is exposed to a wide variety of microorganisms. The neonate’s extrauterine existence is dependant on equilibrium between its own host defense mechanisms and the hostile microorganisms in its environment.

The host defense mechanisms begin to develop early in gestation, but many of them do not function as efficiently at birth as they do in the older infant, child or adult. The immaturity of the immune system becomes apparent in light of the high incidence of infectious disease during the perinatal period. Neonatal sepsis occurs in 1 to 21 infants per 1,000 live births. Identifying and caring for the infected newborn can be one of the greatest challenges for modern neonatal care providers, with mortality rates as high as 30% to 69% of affected infants. Developing countries have both the highest incidence and the highest mortality rates. Many attempts have been made to devise accurate and sensitive clinical and laboratory indices to identity infants likely to have sepsis. None of these have been totally successful. Nurses are often the first to recognize that there is something wrong with an infant and subsequently the symptoms are investigated. Usually, treatment is begun once a presumptive diagnosis of infection is made.


The following terms are used to describe neonatal sepsis.

  • Infection – the body’s response to the invasion of any microorganism, including bacterial, fungal, protozoan, or viral agent, that causes clinical signs of infection.
  • Clinical signs of infection – generalized signs and symptoms seen with any infectious process, including respiratory distress, lethargy or irritability, poor muscle tone, feeding intolerance, apnea, bradycardia, tachycardia, pallor, cyanosis, poor perfusion, and temperature instability.
  • Maternal risk factors – factors that when present increase the risk for infection to the infant and are associated with an increased risk of early-onset sepsis in the infant. These include prolonged rupture of membranes (PROM) > 18 hours, maternal fever, chorioamnionitis, maternal vaginal culture positive for group B streptococcus, history of a previous infant with group B streptococcus disease, and premature delivery < 37 weeks gestation.
  • Sepsis – a bacterial bloodstream infection identified by one or more positive blood cultures in the presence of clinical signs of infection.
  • Early-onset sepsis – sepsis that occurs within the first 3 days of life. It is associated with birth canal organisms acquired in utero or during delivery. Group B streptococcus remains the primary causative agent. One or more maternal risk factors are usually present. Term and preterm infants often present with respiratory distress, which can progress quickly to multisystem involvement within the first 24 hours.
  • Late-onset sepsis – sepsis that occurs after the first 3-5 days of life and is associated with nosocomially acquired microorganisms. It occurs more frequently in premature and low birth weight  (LBW) infants and often includes meningitis. Coagulase-negative staphylococci are the primary causing bacteria. Presentation of signs of infection is slow and insidious.
  • Mixed Non-Specific Presentation- sepsis may present at any time and may present with septic arthritis, osteomyelitis, cellulites, omphalitis, breast abscess, conjunctivitis, myocarditis, endocarditis, otitis media, scalp abscess, UTI or impetigo.


There are many reasons for the increased susceptibility of the newborn to widespread infection. The infant’s birth weight, chronologic, and gestational age at the onset of sepsis also has an impact on the expected mortality rate. Between 5% and 50% of infants with early-onset sepsis will succumb compared with a mortality rate of 10% to 20% with late-onset sepsis. The rate of sepsis in term infants in 0.8 cases per 1,000 live births, and the mortality rate is 2.3%. Two or more maternal risk factors escalate the risk to 4% to 5%.

Low-birth-weight (LBW) infants are at the highest risk for both early- and late-onset neonatal sepsis. This is caused, in part, by mechanical factors such as an increased skin fragility and development of pulmonary atelectasis; immunologic factors such as depressed function of neutrophils, lack of prior exposure to illness and dependence of the fetal antibody spectrum upon that received from the mother; and a prolonged hospital stay with increased exposure to the neonatal intensive care unit (NICU) environment, including various invasive devices and procedures. The National Institute of Child Health and Human Development (NICHD) found that of very low-birth-weight (VLBW) infants, 19 cases of early-onset sepsis per 1,000 live births and 25 cases of late-onset sepsis per 1,000 live births in infants 401 and 1,500 grams. Fifty percent of infants weighing between 405 and 750 grams developed late-onset sepsis.


The organisms responsible for neonatal infection have changed over the past 60 years, and there are marked regional variations. Today, microorganisms commonly responsible for early-onset infection include streptococci, Listeria monocutogenes, and gram-negative enteric rods. Late-onset infections are most often caused by staphylococci, Pseudomonas, or Bacteroides fragilis (anaerobes). After 7 days of age, the nosocomial influence of organisms is important to consider. These organisms include Staphylococcus epidermidis, particularly with invasive tubes or lines; S. aureus (common skin contaminant); and the spectrum of gram-negative bacilli: Klebsiella, Pseudomonas, Serratia, and E. coli. Preterm infants are often affected by repeated bouts of sepsis. Often the organism is unidentified by blood culture, but is simply responsive to antibiotic treatment. Escherichia coli and Group B streptococcus account for 70 percent of all infections.

Other agents of neonatal bacterial sepsis

Gram positive - cocci

Gram negative

Group A streptococcus

Neisseria meningitis

Group B streptococcus

Neisseria gonorrhoeae

Group D strep (streptococcus faecalis)

Branhamella catarrhalis



Staphylococcus aureus (coagulase +)


Staphylococcus epidermidis (coagulase -)



Gram positive – rods

Gram negative – rods

Listeria monocytogenes

Haemophilus influenza

 Anaerobes –

  • Clostridium difficile
  • Clostridium perfingens
  • Clostridium botulinum
  • Clostridium tetani
  • Bacillus cereus
  • Corynebacterium diphtheriae

Enterobacteriaceae –

  • Shigella  
  • Klebsiella
  • Escherichia coli
  • Proteus
  • Salmonella
  • Pseudomonas

Gram positive – rods

Gram negative – rods

Listeria monocytogenes

Haemophilus influenza


Predisposing Risk Factors

One of the predisposing newborn risk factors for infection is Prematurity. Premature infants are far more likely to be jeopardized by the invasion of foreign agents. Because of being born too soon, these infants have missed out on passive transmission of maternal exposure to antigens and subsequent creation of an antibody defense system. Also, the cellular immune system is not well developed in the preterm infant exhibiting decreased phagocytic cellular defenses

Prolonged rupture of the fetal membranes (PROM) is a well-known risk factor for the development of infection. The fetus is at increased risk because the break in the amniotic sac provides a pathway for the migration of organisms up the vaginal vault. The current trend permitting PROM to persist in the presence of a preterm fetus creates the potential environment for bacterial proliferation and subsequent neonatal infection. Many facilities have guidelines for mandatory septic work-up for all preterm infants with PROM and term infants with prolonged rupture of membranes.

A mother with a fever or who has been ill prior to delivery can pass the infection on to her infant. If a maternal temperature of 101?F is noted at delivery, a septic work-up is indicated. Maternal cervical or amniotic fluid cultures may be necessary to determine the causative agent of elevated temperature. If maternal illness suggests viral infection, neonatal viral cultures should be drawn. Early identification of causative agents in the mother may help in the management of the infant.

The presence of foul-smelling amniotic fluid is an indication for neonatal antimicrobial therapy in symptomatic infants. Routine blood cultures and a complete blood count with differential are indicated for identification of neonatal infection. Under these circumstances, the placenta should be sent for pathologic evaluation.

Other risk factors known to be associated with neonatal infection are antenatal or intrapartal asphyxia, iatrogenic complications of treatment modalities, and postnatal invasive procedures. A predisposition to develop sepsis has been noted in low birth weight babies, placed on Indomethacin therapy for treatment of patent ductus arteriosus. Stress in any form inhibits the newborn’s ability to fight infection for several reasons. It increases the metabolic rate, thus requiring more oxygen and energy to support or sustain the body’s vital functions. If the newborn is severely compromised and the oxygen levels continue to be low, regional tissue damage can result. Ischemic or necrotic areas in the lungs, heart, brain or gastrointestinal system provide a receptive environment for colonization and overgrowth of normal bacterial flora. This overgrowth of bacteria is one of the most common sources of neonatal sepsis. Damaged tissue can be repaired only if the infectious process is reversed and adequate tissue perfusion is restored.

There are several known maternal factors associated with neonatal sepsis and infection: low socioeconomic status, malnutrition, no prenatal care, substance abuse, rupture of membranes prior to 37 weeks, substance abuse, presence of urinary tract infection at delivery, peripartum infection, clinical amnionitis, and general bacterial colonization. Neonatal risk factors include antenatal, intrapartum stress (perinatal asphyxia), congenital anomalies, male sex, multiple gestations, concurrent neonatal disease processes, Prematurity, immaturity of the immune system, invasive admission procedures, and antimicrobial therapies.

Summary of risk factors

  1. Preterm labor
  2. Prolonged rupture of membranes > 12-18 hours (the loss of intact membranes allow vaginal bacterial direct access to the fetus)
  3. Maternal fever – chorioamnionitis, maternal septicemia transient bacteremia
  4. Multiple gestation
  5. Previous infected infant
  6. Prematurity
  7. Premature rupture of membranes
  8. Birth asphyxia (hypoxia and acidosis may depress immune cellular functions)
  9. Coitus occurring close to delivery carries an uncertain risk for maternal colonization and ultimately for fetal or neonatal infection
  10. Post natal procedures such as intubation, chest tube insertion and catheterization of umbilical vessels

Clinical Manifestations

Signs and symptoms that are identified in an infected newborn include hypothermia, the inability of the neonate to maintain temperature in the neutral thermal zone (usually between 97.7 and 99?F axillary). Newborns do not have febrile mechanisms. Premature infants often present with a low body temperature as illness ensues. Hyperthermia can occur in term newborns, with temperatures over 100.1?F, but is relatively rare in preterm infants.

An infected infant often presents with lethargy, poor feeding, and perhaps a poor Moro reflex. The infant may eat well in the morning, but by evening suckles poorly or has residuals if being gavage fed. A newborn that is beginning to focus energy on fighting off an infection may have abdominal distention, delayed gastric emptying time, and perhaps diarrhea or loose green or brown stools. Over a longer period, it may be identified that a particular infant has poor weight gain. Hypoglycemia or hyperglycemia, as well as glycosuria, is often a sign of a septic infant who is unable to compensate for the overload of an invasion of infectious organisms. Small preterm infants who are septic often present early with problems handling glucose loads.

Vascular perfusion is typically affected when an infant is septic. Often, a sick neonate will appear gray, mottled, or ashen in color. A sick infant may have poor perfusion and hypotension. Infants can present as cyanotic and can develop Petechiae and potentially, thrombocytopenia. Infections can cause Disseminating Intravascular Coagulopathy (DIC), thereby affecting the prothrombin time, partial thromboplastin time and split fibrin product laboratory values of the newborn. Neonates can subsequently develop a hemolytic anemia, thereby significantly affecting oxygen-carrying capacity in the tiny preterm infant.

Apnea in a term infant in the first few hours of life can be a serious sign of inability to regulate the brain’s respiratory center. Respiratory distress can be an early sign of pneumonia and needs to be considered carefully. A preterm infant who demonstrates apnea in the first 24 hours of life is likely to be infected with foreign organisms. Shock can be a sudden clinical sign of fulminant sepsis and demands immediate attention, even to the extent of double volume exchange or WBC or granulocyte transfusion.

An infant who has bradycardia for unexplained reasons may be sending a signal of possible sepsis. Sclerema and sudden purpura, rash or Petechiae can also be early signs of sepsis. Signs and symptoms that are identified in the infected infant are listed below.

  1. CNS –
    1. Lethargy and/or irritability
    2. Early and persistent apnea (at less than 24 hours of age)
    3. Fever
    4. Temperature instability
    5. Warm trunk with cold extremities
    6. Poor Moro reflex
    7. Seizures
    8. Poor spontaneous movement
  2. Respiratory
    1. Tachypnea
    2. Grunting
    3. Labored breathing
    4. Apnea
    5. Nasal flaring
  3. Gastrointestinal
    1. Feeding intolerance
    2. Vomiting
    3. Poor feeding
    4. Large (>50%) gastric residuals of prior feeding suggesting ilieus
    5. Diarrhea
    6. Hematochezia
    7. Abdominal distention
  4. Skin
    1. Gram negative bacteria especially pseudomonas, may produce small necrotic lesions on face and trunk
    2. Petechiae
    3. Pustulosis
    4. Edema
    5. Jaundice
    6. Sclerema
  5. Circulatory
    1. Bradycardia
    2. Tachycardia
    3. Hypotension
    4. Cyanosis
    5. Decreased perfusion
  6. Physical exam
    1. Local infections – scalp abscess
    2. Joint immobility
    3. Localized erythema (omphalitis)

Mortality and Morbidity

Mortality in early onset sepsis ranges from 28-55%. More infants survive late onset sepsis but they have horrible long-term outcomes and have a higher incidence of meningitis. Morbidity is 25-50% of infants with late onset sepsis resulting in permanent neurologic sequelae.

Major effects

  • Global or profound mental retardation
  • Spastic quadriplegia
  • Cortical blindness
  • Deafness
  • Uncontrolled seizures
  • Hydrocephalus

Mild effects

  • Unilateral sensorineural hearing loss
  • Borderline mental retardation
  • Spastic or flaccid monoparesis
  • Expressive and/or receptive language delay

Laboratory Data

One of the initial diagnostic clues to infection can be obtained from a complete blood count. A septic infant may demonstrate Leukopenia, especially neutropenia with a cell count of polymorphonuclear leukocytes less than 5000/mm3, or may have a large number of immature leukocytes, in particular bands, with band leukocyte ratio greater than 0:2. The following are indications of bacterial infection.

  1. Increased total neutrophils – neutrophilia
  2. Decreased total neutrophils – neutropenia
  3. Increased immature forms (bands, metamyelocytes, sometimes promyelocytes, and myeloblasts)
  4. Increased band: segmented neutrophils ratio equal to or greater than 0:3, or immature: total neutrophils greater than or equal to 0:2.
  5. Presence of Dohle’s bodies (aggregates of reticuloendothelial system)
  6. Presence of vacuoles in nucleus
  7. Toxic granules in cell
  8. Rise in C-reactive protein

The diagnosis of sepsis in a newborn is very difficult to make and is most often based on clinical hunches. The following may be laboratory findings in a septic newborn.

  • Leukopenia, especially neutropenia (< 2000 total neutrophils and bands)
    • Extreme leukocytosis (> 20,000 neutrophils and bands)
    • Increased (> 0.2) ratio of immature neutrophils to mature forms
  • Thrombocytopenia (< 100,000 platelets/mm3)
  • Metabolic acidosis
  • Erythrocyte sedimentation rate (ESR) is not helpful as an isolated test
  • Jaundice (not reliable sign of bacterial sepsis in newborns)
  • Presence of WBC in gastric aspirate obtained shortly after birth indicates amnionitis. The absence of WBC helps in the decision to observe rather than treat some infants.
  • Latex agglutination test for Group B streptococcus (GBS) – urine must be concentrated 25 times and must be free from skin contamination. One-tenth ml of CSF is required.
  • CSF protein 150-200 mg/L for term infants or 300 mg/L for preterm infants is frequently seen.
  • CSF glucose 50-60% or more of blood glucose level

No single clinical sign or single abnormal laboratory test is highly associated with sepsis, but combinations of the above signs strongly suggest sepsis or meningitis. Therefore, a prudent physician identifies infants at high risk and provides for extremely close observation of vital signs and overall status of those children in the first 24 hours of life.

Differential Diagnosis

The organisms responsible for neonatal infection have changed over the past 60 years, and there are marked regional variations. When there is a high index of suspicion of infection, identification of the microorganism and early institution of therapy provides the best outcome. The evaluation for infection generally includes the following components.

  • Obtain blood cultures. The volume of blood should not be less than 10 percent of the culture medium volume.
  • Obtain blood for complete blood count with differential and platelet count.
  • Through a lumbar puncture collect spinal fluid for at least a culture and Gram stain. Gram stain of the cerebrospinal fluid (CSF) can give an indication of the type of microorganism responsible for the infection. Then perform a cell count and protein and glucose determination. Pressure measurement is of little diagnostic use in newborns.
  • It may be wise to alert the clinical laboratory that only a small amount of spinal fluid will be available for analysis.
  • Urine obtained by suprapubic bladder aspiration is unlikely to demonstrate bacteria by culture or Gram stain when obtained immediately after birth. An evaluation for sepsis performed several days after birth should however; include an aspiration as part of the diagnostic evaluation.
  • A chest radiograph is required to rule out pneumonia. The pneumonic pattern of GBS may mimic hyaline membrane disease (HMD). Parenchymal densities must be considered to be pneumonia and treated as such until cultures or clinical course proves otherwise.
  • Other tests that may be useful include latex agglutination or counterimmunoelectrophoresis of urine or CSF, erythrocyte sedimentation rate and acute phase proteins.
  • Other nonspecific findings, such as hypoglycemia, hypocalcemia, thrombocytopenia, hyponatremia, or metabolic acidosis, may also be present.
  • Definitive diagnosis is based on recovery of a microorganism in blood, CSF, urine or other body fluid.

Initial Stabilization

Comprehensive management must include supportive care with fluids, glucose, electrolytes, and support of blood pressure and tissue perfusion. Collaborative management for an infected infant focuses on ventilatory support, oxygen therapy, correction of acidosis, immune therapy, volume expanders, extracorporeal membrane oxygenation if persistent pulmonary hypertension is present, and antimicrobial agents. The exact management plan is based on individual signs, symptoms, and laboratory tests.

The provision of adequate warmth and correction of hypotension, if observed, should be the first priorities of care. Central arterial pressure monitoring should be considered if such monitoring has not been instituted. Long term effects of vasopressor agents on neonates are relatively undocumented, but such agents may be indicated for hypotension and oliguria. Dopamine 5 to 15 mcg/kg/min infused into a secure intravenous site. Assisted ventilation may be necessary if apnea is severe or if sepsis is complicated by severe pneumonia.

The selection of antimicrobials is based on the microorganism present and infant’s response to therapy. Infectious microorganisms fall into two broad classes: gram-positive and gram-negative. The shape of the organism categorizes it as either a coccus or a rod. Generally gram-positive organisms respond to broad-spectrum antibiotics such as penicillin analogues and the first generation cephalosporins, and the beta-lactamase penicillins. The gram-negative microorganisms are most often susceptible to aminoglycosides, cephalosporins and chloramphenicol.

Tests must be run to determine the specific sensitivity of an organism to the antimicrobial selected. Initial antibiotics for infections of undetermined etiology should be ampicillin and gentamycin so that both gram-positive and gram-negative organisms are covered. This combination of antimicrobials has a synergistic effect, increasing the efficacy of either drug therapy used alone. Additional therapy or selection of other agents is necessary if staphylococcal infection is suspected. If staphylococcal infection is strongly suspected, consider methicillin. If staphylococcus epidermidis is recovered in cultures and is resistant to methicillin, then consider vancomycin. The presence of indwelling catheters, the postnatal age of the infant and CSF findings should influence the treatment decisions.

Aminoglycoside antibiotics have poor or variable CSF penetration and are therefore of limited usefulness in gram-negative meningitis. Third generation cephalosporins effectively penetrate the CSF.

Correct coagulation abnormalities, which should be anticipated with significant sepsis of any bacterial etiology or with enter-viral infections. Platelet transfusions, fresh frozen plasma, or cryoprecipitate transfusions for correction of abnormal prothrombin or partial thromboplastin times are indicated based on the specific abnormalities detected and local availability of these products.

If sepsis is suspected in the presence of “soft signs” of infection, then cultures should be obtained and antibiotics given for a minimum of 3 days while awaiting culture results.

Management of Overwhelming Sepsis and Pneumonia

A “healthy-appearing” neonate with bacteremia can become an infant in septic shock within a few hours. An early sign of untreated sepsis is death. The findings of overwhelming sepsis in neonates include respiratory failure, acidosis, extremely poor perfusion, hypotension, grunting respirations, evidence of hemorrhage petechiae, purpura, pulmonary bleeding, neutropenia and eventually sclerema. These infants lack specific antibodies in their pool of trans-placentally acquired immunoglobulin. This limits the ability of the neutrophils to ingest and destroy bacteria. The extremely rapid growth of common infecting agents (Group B streptococcus, E-coli) may create such a large body burden of organism that relative antibiotic resistance results. Toxins already circulating may cause profound cardiopulmonary changes that are unresponsive to treatment.

Because of the extremely high mortality of such infants, several ancillary therapies have been tried in addition to the conventionally accepted treatments of assisted ventilation, crystalloid fluid administration, and infusions of bicarbonate, antibiotics and vasopressor agents. The first of these approaches consists of treatment to replace or supply specific immune factors. This may mean granulocyte transfusions in infants with neutropenia and total body depletion of neutrophils reflects in absent or decreased bone marrow stores, or infusion of pooled adult hyper immune globin to try to collect specific antibody defenses.

The second approach is to correct these defects and alter the oxygen-hemoglobin characteristics and oxygen tissue delivery characteristics of the infant’s blood by complete exchange transfusion.

Congenital Infections

The microorganisms most often responsible for congenitally acquired infections have been grouped together as the TORCH infections. These include toxoplasmosis, others, rubella, cytomegalovirus, and herpes. The “others” category includes various microorganisms that have been responsible for congenital infections. However, the list of microorganisms implicated in congenital infections has grown, so the acronym is no longer inclusive. It is still used to mean all infections acquired by the fetus in utero.

Acute toxoplasmosis in a pregnant woman often goes undetected and undiagnosed. Maternal transmission occurs from consumption of poorly cooked meat, or by ingestion of infected cat feces. Risk of transmission is highest in the 3rd trimester.  First trimester transmission usually ends in spontaneous abortion. Clinical questioning after the identification of an infected infant often leads to reflection and memories of a period of enlarged lymph nodes and fatigue but no fever. Women often report a mononucleosis-like syndrome that may have a febrile course, with malaise, headache, fatigue, sore throat, and sore muscles.

In an infant, toxoplasmosis can present with hydrocephalus, chorioretinitis, and intracranial calcification. There are an incredible variety of clinical signs in the scope of the disease. A normal picture at birth, or even severe erythroblastosis, hydrops fetalis, and other clinical signs can occur. Neurological signs similar to encephalitis may be the only significant presentation of this clinical problem, including seizures, bulging fontanels, nystagmus, and abnormal increase in circumference of the head. If the infant is treated, signs and symptoms may disappear, allowing normal cerebral growth and development.

In term infants, delayed disease may occur in the first 2 months of life and is usually milder. Clinical signs may be generalized sepsis, enlarged liver and spleen, late-onset jaundice, enlarged lymph nodes, or late-onset central nervous system problems, including hydrocephalus and eye lesions. Infants with congenital toxoplasmosis may have new lesions appearing until age 5 years.

The typical presentation of the rubella virus is mild, with malaise, low-grade fever, headache, and conjunctivitis. In 1 to 5 days, a macular rash appears on the face and usually disappears after 3 to 4 days. Natural viremia is necessary for placental and fetal primary disease. Most cases occur following primary disease. Skin rashes that resemble rubella may occur as a result of adenovirus, enterovirus, or other respiratory virus infections. Laboratory titers are recommended to confirm the diagnosis of rubella infection since there is a strong possibility of subclinical infection. It takes about 4 to 6 weeks to obtain clinical confirmation of rubella isolation. The detection of rubella antibody confirms the presence of the infection.

A fetus infected with rubella often has cardiac defects and deafness. The central nervous system seems particularly vulnerable to the rubella virus especially if the virus is acquired prior to the first 16 weeks of gestation. Congenital rubella syndrome is described by the CDC as hearing loss, mental retardation, cardiac malformations, and eye defects. The rubella virus can slow cell replication. This causes intrauterine growth retardation and a failure of cell differentiation during fetal organ formation. Tissue damage seems to occur from the inflammatory response to the infection. Myocarditis, pneumonitis, hepatosplenomegaly and vascular stenosis can also be present. As seen with other severe congenital infections, signs and symptoms may continue to develop until 10 or 20 years of age. Late clinical signs of this disease include insulin-dependant diabetes, thyroid abnormalities, hypoadrenalism, hearing loss, and eye damage.

Cytomegalovirus (CMV), a member of the herpes family, is a very common infection. More damage occurs to the fetus when the exposure to and acquisition of CMV occur from a primary lesion. Congenital CMV occurs in about 0.2 to 2.2 percent of all newborn infants. Primary lesions cause intrauterine growth retardation, microcephaly, periventricular calcifications, deafness, blindness, congenital cataracts, profound mental retardation, hepatosplenomegaly, and jaundice. A characteristic pattern of Petechiae, called “blueberry muffin” syndrome, is associated with congenital CMV. Severe complications at birth are seen in approximately 5 percent of congenital infections. Urine culture for CMV is the most rapid and sensitive indicator of infection. IgG and IgM antibody titers are also indicated. Elevated IgM levels alone denote exposure to CMV but are not diagnostic because there is no method to determine the timing of the exposure. Elevate IgG titers indicate perinatally acquired CMV infection. Transmission of CMV via infected blood products has been significantly decreased through the use of CMV-negative donors or irradiation of blood products. Premature and low birth weight infants are especially vulnerable to the infusion of this virus in blood products. The best method of prevention is the institution of standard precautions, including good hand washing.

When newborns acquire syphilis from hematogenous spread across the placenta, the effects are on the major organ systems of the fetus, especially the central nervous system. Common presentations of the infected infant are hepatosplenomegaly, jaundice, low birth weight, intrauterine growth retardation, anemia, and osteochondritis. There is often a bilaterally superficial peeling of the skin on the neonatal palms and soles. Nonimmune hydrops is a very common presentation in congenital syphilis. The symptomatology of perinatal syphilis is similar to that of any other viral infection that spreads hematogenously from the mother to the placenta and on to the developing fetus. A lumbar puncture for CSF analysis and radiographs of the long bones facilitate the definitive diagnosis. Congenital neurosyphilis is always a consideration, and the CSF should be examined for the presence of spirochetes. X-ray changes such as blurring of the epiphyseal borders demonstrate recent fetal infection, and periostitis represents prolonged involvement.

Acquisition of herpes simplex virus in utero can result in spontaneous abortion, preterm birth, or a normal baby. Manifestations of the disease are very broad. The clinical presentation of the congenital acquisition of the infection includes skin vesicles and/or scarring, hypopigmentation, chorioretinitis, microcephaly, and hydraencephaly. Greater than 20 percent of the newborns with disseminated disease do not develop skin vesicles, making identification of positive infants more difficult. Laboratory tests are the most common way to differentiate HSV from other bacterial and viral infections. The most rapid method includes a cytologic exam. Routine cultures should include any vesicles on the skin; oropharyngeal or eye secretions; or stool. Viral typing is only done for epidemiologic purposes. Intrapartal transmission is more likely to occur in the presence of ruptured membranes. Other risk factors include intrauterine fetal monitoring (scalp electrodes and intrauterine pressure catheters) and fetal scalp sampling. It is not recommended that women infected with HSV be monitored by these methods. Transmission from mother to infant from an infected breast lesion and from oral lesions has been reported.

Varicella is the member of the herpes virus family that commonly causes chicken pox as well as varicella zoster. Most women of childbearing age have been exposed to or have contracted this virus; those that have not should receive the varicella vaccine prior to pregnancy. Symptoms of varicella are usually present 10 to 20 days after exposure and include fever, malaise, and an itchy rash. The maculopapular rash eventually forms vesicles and crusts over. Potential complications include pneumonia, encephalitis, arthritis, and bacterial cellulitis. If the virus is contracted early in pregnancy, the damage is likely to be cutaneous musculoskeletal, neurological and ocular. Infants can have intrauterine growth retardation, microcephaly, cerebellar and cortical atrophy, cataracts, and chorioretinitis. Viral infection in the last 3 weeks of pregnancy will infect one in four newborns. The severity of newborn disease is determined by the timing of the exposure. Infections are generally severe if contracted within 4 days before delivery and 2 days after delivery. Severe viral respiratory distress with significantly depleted maternal passive antibody transmission puts the infant at an even greater risk for other complications.

Gonorrhea appears most frequently in young adults, ages 15 to 24 years. Symptoms are mild but in the pregnant woman can cause inflammation and weakening of the fetal membranes and early rupture. Gonococcal conjunctivitis in the newborn has historically been a risk from transmission via the birth canal. Prophylaxis has been mandated by law, with the use of silver nitrate 1 percent solution or erythromycin in both eyes at birth.Fetal scalp electrodes have been identified as a potential method of organism transmission to the fetus.

Hepatitis B Virus (HBV) infection early in pregnancy causes 50 percent risk of neonatal HBV and 90 percent at risk to develop HBV by their first birthday. Untreated infants are likely to become carriers, which may eventually lead to primary hepatocellular carcinoma. Treatment for these infants should be HBV vaccine with hepatitis B immunoglobulin. Prematurity, low birth weight and hyperbilirubinemia are clinical signs of HBV infection. Hepatosplenomegaly is also a common presenting symptom of an infant that is infected. An infected infant may be asymptomatic or present with a picture of fulminant sepsis.

Human Papilloma Virus (HPV) – genital warts or condylomata acuminate can cause laryngeal papillomatosis in the newborn demonstrated by a weak cry or hoarseness if the mother is not treated. The newborn may have stridor or other respiratory symptoms. The presence of these warts during vaginal delivery can be extremely uncomfortable. Intrapartal transmission is possible if the warts are visible. Prenatal treatment is associated with low complications and recurrence rate. The treatment alleviates the need for a cesarean delivery. Examination, treatment and follow-up of sexual partners are important aspects of treatment, because 50 percent of partners are infected.

Chlamydia is a bacterium that grows between cells. It is one of the most common sexually transmitted diseases. Chlamydia conjunctivitis can present in the newborn with a very watery discharge that may progress to purulent exudates. Application of erythromycin ointment at birth for ocular prophylaxis will successfully treat both Chlamydia and gonococcal conjunctivitis. Pneumonia can occur in newborns that have contracted Chlamydia from their mother’s genital tract. Typical presentation is tachypnea, barrel chest, and an increased oxygen requirement. The infant may have interstitial infiltrations, hepatosplenomegaly, and increased eosinophils. Diagnosis is based on physical examination and conjunctivitis.

Respiratory Syncytial Virus (RSV) is an infection usually found in older infants. Maternal antibodies protect the infants for the first few weeks of life, but as passive immunity diminishes, these infants become more vulnerable. Premature infants, already immunocompromised, are more susceptible to the virus during the prolonged hospitalizations. Infants infected before 4 weeks of age may be asymptomatic or have an upper respiratory infection with fever, bronchiolitis, apnea and pneumonia. Nosocomial transmission between caretakers is possible.

Adenovirus and Rotavirus can be enteric and can cause significant viral gastroenteritis. Breastfeeding can protect against these organisms. Early signs of illness include lethargy, irritability, and poor feeding followed by passage of watery yellow or green stools free of blood but containing mucus. Vomiting and slight fever may accompany the diarrhea. Rotavirus has been shown to cause necrotizing enterocolitis.

Candida albicans is a fungus that may result from prolonged broad-spectrum antibiotic use in small premature infants. Yeast infections can localize in any organ system. Administration of hyperalimentation, frequent use of indwelling venous lines, and invasive procedures may also predispose the infant to Candida. The infants may present with thrush or cutaneous (perianal area) or acute disseminated candidiasis (systemic infection). The infant presents with signs and symptoms of sepsis often worsening with no presence of positive cultures. The infant may have respiratory distress, abdominal distention, guaiac-positve stools, carbohydrate intolerance, candiduria, temperature instability and hypotension. Cutaneous infection may be treated with Nystatin but systemic infection requires treatment with Amphotericin.

HIV/AIDS offers the infant 3 modes of transmission: a) transplacental, b) intrapartal where there is exposure to maternal blood and vaginal secretions, c) postnatal through maternal secretions like breast milk. HIV causes immunosuppression in the neonate. An HIV mom is more susceptible to other opportunistic organisms, such as CMV and HSV, both of which put the infant at risk. Neonates born to HIV positive mothers are usually asymptomatic. Infant’s symptoms usually don’t appear until 4-6 months of age. These later symptoms include: failure to thrive, persistent thrush, hepatosplenomegaly, recurrent diarrhea, recurrent bacterial infections, and hepatitis. These infants should be treated immediately after birth with AZT if mothers HIV status is known. If the mother was treated during pregnancy with AZT, the baby has a better chance of not getting the virus. Immunizations for HIV exposed infants should NOT be live virus.

Nosocomial Infections

Both colonization and infection are nosocomial events, meaning “of or related to a hospital.” The common meaning of the term nosocomial is “hospital acquired.” Nursery-acquired infections are reported to the Center for Disease Control, which has a National Nosocomial Infections Surveillance System.

The incidence of nosocomial infections in NICUs is 5 to 25 percent. Infants who are critically ill remain in a pathogen-filled environment are often in jeopardy because of their prolonged length of stay in the hospital. Mortality associated with these infections is anywhere from 5 to 20 percent, depending on the geographic area and specific weight groups.

Coagulase-negative staphylococcus has been identified as a major cause of nosocomial infections. Low birth weight, multiple gestation, and prolonged hospitalization are significant factors for nosocomial infection. Yeast infections often occur if previous antibiotic therapy has been given. This infection is also associated with colonization of vascular catheters, assisted ventilation, and necrotizing enterocolitis.

Nursery epidemics can be caused by gram-negative and gram-positive or viral organisms because they have the ability to colonize or infect human skin or the gastrointestinal tract; the ability to be carried from person to person by hand contact; and characteristics that allow existence on hands of personnel or in fluids or on inanimate objects, including intravenous fluids, respiratory support equipment, solutions used for medications, disinfectants, and banked breast milk.

Resistance to antibiotics is a very serious problem in many NICUs particularly with gram-negative enteric pathogens. Aminoglycoside resistance is a problem in many urban nurseries, as well as colonization and infection with methicillin-resistant staph aureus. Respiratory infections, including RSV, influenza virus, Para influenza virus, rhinovirus, and echovirus, have occurred in many nurseries. These are more difficult to identify and thus more difficult to report. CMV (cytomegalovirus) infection has been reported as transfusion-related problem in low birth weight infants and thus has prompted the current policy using CMV-screen donors. Hepatitis A has also been reported as a transfusion related problem that may develop in infants and staff in NICUs. Thus, almost any organism given the right environment and support can become a nosocomially transmitted infection.

Infection Control Policies

The hospital infection control committee based on the recommendations of the American Academy of Pediatrics and the Centers for Disease Control should set policies and procedures in nurseries. The significance of these policies to newborns should be detailed in a hospital policy book. The following topics should be covered.

  • Ocular prophylaxis
  • Skin and cord care
  • Nursery staff
  • Nursery design and environment
  • Hand washing
  • Staff apparel
  • Isolation
  • Visitors
  • Employee health
  • Epidemic control


Many factors place the neonate at high risk for infection. The nurse is in a unique role to implement methods for prevention of infection in nurseries, to detect early signs and symptoms of infection, and to participate in infection control. An understanding of risk factors, methods of perinatal transmission, microorganisms, signs and symptoms of infections, and appropriate therapy provides the healthcare providers with a sound basis for management of care as well as the development of hospital infection control policies for the NICU.


Baker, C.J. and Edwards, M.S. (2000) Group B Streptococcal Infections. Infectious Diseases of the Fetus and Newborn, 5th Ed. Remington, J.S. and Klein, J.O. (eds.) W.B Saunders Company: Philadelphia.

Brueggemeyer, Ann; Kenner, Carol and Gunderson, Laurie Porter; Comprehensive Neonatal Nursing – A Physiologic Perspective, W.B Saunders Company, Philadelphia. (2003)

Hengst, Joan M., The Role of C-Reactive Protein in the Evaluation and Management of Infants with Suspected Sepsis; Advances in Neonatal Care, Vol. 3 No. 1 (February 2003) pp. 3-13.

Hodson, W. Alan and Truog, William; Critical Care of the Newborn, W.B. Saunders Company, Philadelphia. (2000)

Johnson, Terry S. Perinatal Presentations of Group B Strep, Lodestar Enterprises, Inc. (2000)

Mahlmeister, Laura; Perinatal Group B Streptococcal Infections – A Nurse’s Role in Identification and Prophylaxis, The Journal of Perinatal and Neonatal Nursing; Vol. 10 No. 2 September 1996.