Mrs. Hartley is the Education/Employee
Health Coordinator at Lake City Medical Center. She received
her Masters Degree in Perinatal Nursing from Indiana University/Purdue
University at Indianapolis. She has 3
years experience in Staff and Patient Education; 28 years clinical experience
that include almost 20 years of Neonatal Intensive Care. She is certified in
High Risk Neonatal Nursing and Fetal Monitoring.
purpose of this course is to update healthcare professionals on how to identify
and manage neonatal infections.
completion of this module the reader will be able to:
risk factors associated with neonatal infections,
organisms responsible for neonatal infections,
types, timing and clinical presentations seen in infants with sepsis,
management of neonatal sepsis, and
that can cause congenital infections.
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 mothers uterus. However, during the birth process and
subsequently, the neonate is exposed to a wide variety of microorganisms. The
neonates 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.
the bodys response to the invasion of any microorganism, including
bacterial, fungal, protozoan, or viral agent, that causes clinical signs
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
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
a bacterial bloodstream infection identified by one or more positive blood
cultures in the presence of clinical signs of infection.
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.
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.
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 infants
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.
agents of neonatal bacterial sepsis
Gram positive - cocci
Group A streptococcus
Group B streptococcus
Group D strep (streptococcus
Staphylococcus aureus (coagulase +)
Staphylococcus epidermidis (coagulase
- Clostridium difficile
- Clostridium perfingens
- Clostridium botulinum
- Clostridium tetani
- Escherichia coli
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 newborns ability to fight infection for
several reasons. It increases the metabolic rate, thus requiring more oxygen
and energy to support or sustain the bodys 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
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
rupture of membranes
8. Birth asphyxia
(hypoxia and acidosis may depress immune cellular functions)
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
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
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
brains 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.
b. Early and
persistent apnea (at less than 24 hours of age)
e. Warm trunk
with cold extremities
Poor Moro reflex
e. Nasal flaring
c. Poor feeding
(>50%) gastric residuals of prior feeding suggesting ilieus
a. Gram negative
bacteria especially pseudomonas, may produce small necrotic lesions on face and
e. Decreased perfusion
6. Physical exam
infections scalp abscess
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
Global or profound mental retardation
sensorineural hearing loss
Spastic or flaccid
receptive language delay
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.
total neutrophils neutrophilia
total neutrophils neutropenia
immature forms (bands, metamyelocytes, sometimes promyelocytes, and
band: segmented neutrophils ratio equal to or greater than 0:3, or
immature: total neutrophils greater than or equal to 0:2.
of Dohles bodies (aggregates of reticuloendothelial system)
of vacuoles in nucleus
granules in cell
- Rise in
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.
especially neutropenia (< 2000 total neutrophils and bands)
Extreme leukocytosis (> 20,000 neutrophils and bands)
Increased (> 0.2) ratio of immature neutrophils to mature
(< 100,000 platelets/mm3)
sedimentation rate (ESR) is not helpful as an isolated test
(not reliable sign of bacterial sepsis in newborns)
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.
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.
protein 150-200 mg/L for term infants or 300 mg/L for preterm infants is
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.
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
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
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
Definitive diagnosis is based on recovery of a microorganism
in blood, CSF, urine or other body fluid.
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 infants 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
Aminoglycoside antibiotics have poor
or variable CSF penetration and are therefore of limited usefulness in
gram-negative meningitis. Third generation cephalosporins effectively penetrate
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.
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 infants blood by complete exchange
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
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
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 mothers 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
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. Infants symptoms usually dont 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.
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.
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
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.
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.
Skin and cord care
Nursery design and environment
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 Nurses Role in Identification and Prophylaxis, The Journal of
Perinatal and Neonatal Nursing; Vol. 10 No. 2 September 1996.