Neonatal Infections

Janet Wong, M.D.

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Typical Syndrome of Congenital Infection
SGA (Small gestational age) or intrauterine growth retarda-
tion is characterized by jaundice, chorioretinitis,
hepatosplenomegaly microcephaly, and hydrocephaly which
are the direct result of the congenital infection and microbial
invasion. By contrast, eye defects and cardiac defects are
caused by cell death or chromosomal damage.

Feature Comment

SGA Causal relationship exist for rubella,

CMV, toxoplasmosis

Hepatosplenomegaly Reflects microbial invasion and

proliferation (not a defect in
Jaundice organogenesis)
Chorioretinitis

Eye defects Cause by cell death or chromo-

Cardiac defects somal
damage

Microcephaly Consequence of lesions from con-

Hydrocephaly genital infection rather than
teratogenesis

2
 Signs Common to Congenital Infec-
Signs common to congenital infections include purpura,
tions jaundice, hepatosplenomegaly, pneumonitis,
meningoencephalitis. They are not all present in every pa-
tient within congenital infection, but any of these features can
be associated with various etiologies. They are common to
• Purpura, jaundice, hepatosplenomegaly, pneumonitis, rubella, cytomegalovirus, herpes simplex virus, Coxsackie B
infections, Toxoplasma, and syphilis.
meningoencephalitis
• Common to rubella, CMV, HSV, Coxsackie B, T. gondii, T.
pallidum

3
 Typical Clinical Manifestations of Con-
genital Infections
With syphilis you sometimes see an exanthem characteristic
of syphilis. If you saw that you would immediately think of
syphilis, whereas many of the others do not have an
exanthem. None of them commonly have an exanthem,
although some might have one.

Sign Rubella CMV Toxo Syphilis Another feature of diagnostic significance is the presence of
intracranial calcifications which would suggest CMV. Keep in
Hepatosplenomegaly + + + + mind also toxoplasmosis, although a less common congeni-
Jaundice + + + + tal infection, also can give you intracranial infections,
whereas if you had that finding of intracranial calcification,
Exanthem - - + ++ your patient and you were thinking about syphilis or rubella,
you would not think that would be etiologically compatible.
Purpura/petechiae + + + +
Hydrocephalus + + ++ -
Microcephaly - ++ + -
Intracranial calcifications - ++ ++ -
Heart defects ++ - - -
Bone lesions ++ - - +
Glaucoma ++ + - +
Chorioretinitis ++ + ++ +
Cataracts ++ - + -

4
 Parvovirus B19
• About 50% of childbearing-aged women are immune
• After household exposure, ~50% of susceptibles become
infected
• Risk of presumed parvovirus-related fetal death from
household exposure in first 20 weeks of pregnancy is 3-9%
• Risk alter 20 weeks of pregnancy is unknown; 3rd trimester
infection may cause newborn anemia
Parvovirus B19. About 50% childbearing-age women are
immune to the parvovirus but that means the other half are
nonimmune and therefore susceptible. If a woman has a
household exposure, we know that about 50% of the
susceptibles in a household will become infected. There is a
parvovirus B19 infection. So if a woman is pregnant and her
two-year-old comes home with classic erythema infectiosum,
she has about a 50% chance if she is susceptible of becom-
ing infected.
The risk of presumed of parvovirus-related fetal death from
household exposure in the first 20 weeks (early in preg-
nancy) is estimated at 3% to 9%. By contrast, after 20 weeks
of gestation, the risk is absolutely unknown. It is estimated at
less than one-percent.
Third trimester infection may cause some newborn anemia,
but usually this is not the hydrops fetalis type of scenario.
5
 Parvovirus B19
• Virus causes fetal anemia, heart failure and death (hydrops
fetalis)
• Risk of fetal death after occupational exposure is low (<1%)
• No association with fetal anomaly
Viruses causing fetal anemia. If you have an early gestation
exposure, say 18 weeks, you may end up with fetal anemia,
secondary heart failure, and in utero death with the fetus that
shows all the histopathologic features of hydrops fetalis. The
risk of fetal death after occupational exposure is low. Most of
the times the hospital’s employee has been shown to be
seropositive and, therefore, not at risk.
6
 Diagnostic Evaluation for Congenital
One of the things to remember about provirus is that we do
Infection have serologic tests, and if a question comes up about
somebody being susceptible, you are going to have to do a
serologic test. If the person has an immunity to parvovirus,
then they are not susceptible then you do not have to deal
• Rubella with these pregnancy-related issues. If they are pregnant,
depending on the time of gestation, you can at least counsel
• Virus Culture: Nasopharynx is the most reliable site; the patient, based on the gestation, about potential risk.

conjunctivae, CSF or urine also are potential sites

The one thing to remember about parvovirus B19 is that you
• Cord serum for rubella-specific IgM are not going to see fetal anomalies. So this virus is red cell
specific. It causes anemia depending on the time of gesta-
• CSF for rubella-specific tion and the anemia can cause spontaneous abortion or
intrauterine death due to hydrops or presentation of a quite
• Persistence of rubella-specific IgG for 6-12 months CMV
currently ill baby with hydrops fetalis.
• Viral isolation: urine, saliva, tissues
• Rapid viral diagnostic techniques
• Toxoplasmosis
• Demonstration of IgM antibodies to toxoplasmosis in cord
serum or infant serum is diagnostic; IgM antibodies in CSF
supports the diagnosis in CNS infection
• Double sandwich IgM-ELISA method is more sensitive than
IgM-IFA
• IgA antibodies to toxoplasmosis in infant
• Demonstration of Toxoplasma antigens in CSF
• Parvovirus
• Detection of IgM antibodies to parvovirus in infant serum
• Parvovirus-specific PCR

7
Indications for Evaluation of Congeni-
tal Syphilis
• Mother with positive nontreponemal tests confirmed by a
positive treponemal test and:
• Untreated or inadequately treated syphilis
• Treatment in pregnancy with non-penicillin regimen
• Lack of expected decrease in nontreponemal antibody titer
after penicillin treatment
• Treatment <1 month before delivery
• Treatment not documented
• Insufficient follow-up to assess response and current status
Diagnostic evaluation of congenital infection. Rubella can be
cultured if you have access to a virology lab. If you do not,
then the best way to make the clinical diagnosis is to get
cord serum for specific IgG antibody. In patients who have
meningoencephalitis, the spinal fluid actually may have IgM
detectable antibodies too, so there are two specimens that
can be serologically tested for IgM rubella specific antibody.
You can culture this virus if you do have serology laboratory
access, the nasopharyngeal secretions are the most reliable.
IgG comes from the mother and is another serologic piece of
information that is useful in congenitally infected babies. IgG
persists for six to twelve months, and after that time you
know that IgG is being made by the baby because passive
antibody from the mother has gone away by that time.
CMV. The cardinal way to make the diagnosis is isolation of
this virus from a urine specimen. You also may isolate CMV
from saliva or from tissues.
There are a number of rapid viral diagnostic techniques for
CMV. Urine cultures are fairly standard. The virus is not
fastidious and the least expensive and easiest way to make a
specific diagnosis is to grow CMV from the urine.
In order to make the diagnosis of congenital CMV, you have
to have access to your patient in the first two weeks of life
because after that, acquiring CMV becomes a complicated
interpretation problem.
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 Diagnostic Evaluation for Congenital
Syphilis
• Physical examination
• Quantitative nontreponemal serologic test
• CSF analysis for cells, protein, VDRL
• Antitreponemal IgM test
• Long bone x-rays
• Other clinically indicated tests (e.g., CBC, CXR)
Toxoplasmosis. The diagnosis is serologic. Again, we are
not using IgG antibody in any of these congenital infections
because the mother is going to have high levels of IgG that
are transferred to the baby. We are looking for detection of
toxoplasmosis, specific IgM antibodies in cord serum are
tested. If the CNS is involved there is a serologic assay for
cerebral spinal fluid that would support the diagnosis of CNS
infection due to toxoplasmosis. The ELISA is much more
sensitive than the indirect fluorescent antibody test as op-
posed to the IFA. It is a more desirable method because it is
more sensitive.
The IgA antibody test is not a passively acquired antibody, so
the baby has to be making it, and is very helpful as an ad-
junctive serologic piece of information in establishing the
diagnosis of toxoplasmosis.
Parvovirus is a virus that cannot be cultured. Serologic de-
tection of IgM in the infant serum or cord serum is diagnostic.
More and more places are now getting parvovirus specific
PCR.
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 Typical Syndrome of Natally or
Syphilis. Indications for evaluation of patients with congenital
syphilis. The mother with the positive nontreponemal test is
Postnatally Acquired Nonbacterial the RPR or VDRL. The first thing that happens is that we
cannot say that she does not have a biologic false-positive,
Infection so we need to make sure, that if she has a treponemal test,
that it is confirmed with a nontreponemal test. The MHATP is
a common one and you need both of these to make a firm
serologic diagnosis in the mother and the baby.
Sign HSV Enterovirus HBV HIV
For the definitive diagnosis of syphilis you have to have
microscopic evidence of spirochetes, a dark field or direct
fluorescent antibody specimen from some sort of
Hepatosplenomegaly + ++ ++ ++
mucopurulent secretions. The congenitally-infected patient,
Adenopathy - + - ++ unless they have the typical exanthem, the pustule, where
you can open them and they are teeming with spirochetes,
Pneumonitis + + - ++ before you treat the patient and do a dark field on that, all of
Petechiae or purpura + + - - our diagnoses of congenital syphilis is presumptive at best,
and to make the presumptive diagnosis, you have to have a
Vesicles ++ - - - nontreponemal test that is confirmed with a treponemal
antigen test.
Meningoencephalitis + + - +
Paralysis - ++ - - After the mother has confirmed both tests positive, she is
untreated during her pregnancy. Inadequate treatment is a
Myocarditis + ++ - + non-penicillin regimen. Obstetricians are told to desensitize
the patient and treat with penicillin, but that does not always
Conjunctivitis or ++ + - -
happen.
Keratoconjunctivitis
Inadequate treatment would mean a non-penicillin drug or
inappropriate dose, or inappropriate duration. Lack of ex-
pected decrease in VDRL or RPR after the patient has been
treated, and usually what we are looking for is a four-fold or
greater decrease. Treatment less than one month before
delivery is considered inadequate. Treatment is considered
inadequate if it can not be documented. Documented means
that you have documented evidence. The patient saying that
she was treated with penicillin is insufficient to document
treatment. Insufficient follow-up to assess response is con-
sidered inadequate. For example, you may not have access
to a previous serology and you cannot assess her response
to therapy unless you have previous results.

So, once you have decided that the patient needs a diagnos-
tic evaluation based on the mother’s situation, you do a
physical examination, you do a quantitative nontreponemal
serologic test. You do a spinal fluid through a lumbar punc-
ture. You look at the cell count, protein and VDRL. Here we
are in a situation where you really need spinal fluid that does
not have contaminating blood, because if you had contami-
nating blood it is difficult to interpret the protein and the cell
count, it is virtually impossible to do a reliable VDRL when
you have blood in the spinal fluid, you can send a VDRL, and
if it is negative it is informative , but if it is positive you do not
know whether that is from the blood or whether the patient
has neurosyphilis.

There are a lot of babies with completely normal cell counts

and proteins who has positive VDRLs. Then there are some
babies who have abnormal cell counts and abnormal pro-
teins and negative VDRLs. They should all be treated for
neurosyphilis.

The IgM is a test that is not commercially available, but the

CDC will do an IgM test for you. It is reliable for the diagno-
sis. Long bone x-rays are necessary because patients with
congenital syphilis can have a completely normal physical
examination and normal CSF analysis and have the
osteolytic and periosteal elevation changes caused by con-
genital syphilis. This is clinically silent early, but still needs to
be treated.

For hepatitis B virus , babies who are more than a month of

10

Diagnosis of Natally or Postnatally Ac-
quired Nonbacterial Infections
• HSV
• Specimens for culture from vesicle, mouth or throat,
conjunctiva, blood and CSF yield virus in 1-3 days; DFA of
vesicle scrapings or EIA of HSV antigens are specific but
less sensitive
• Enterovirus
• Specimens for viral isolation from throat and rectum and
sites of clinical involvement (CSF, blood, biopsy material)
• HBV
• Detection of HBsAg in infant's serum
age and may have these clinical manifestations; they uncom-
monly present at birth, and for HIV infections, realizing that
any patient can be different; you are not going to see clinical
signs of HIV infection at the time of birth. You are going to
look to these, and so the timings areas at four to six months
of age or somewhat older.
Usually the viral agent is transmitted intrapartum. Typical
findings at presentation, four to six months of age or slightly
older, hepatomegaly, prominent adenopathy; the patient may
have pneumonitis, and this is not an opportunistic infection,
but usually the lymphoid intrastitial pneumonitis syndrome
that we see typically with HIV.
One comment about enteroviruses, is where as we see a
disseminated fulminant presentation with
hepatosplenomegaly, adenopathy, coagulopathy and often
death. They may have very helpful clues to this presentation,
with paralysis or myocarditis. That may help the clinician,
but those are very ominous presentations because we do not
have specific therapies for enteroviral disease and those
patients typically do quite poorly.
Diagnosis for HSV. For the patient that presents with the
vesicle this is the most accessible way to have rapid viral
diagnosis by culture virus. Without skin vesicles present, the
mouth or throat, the conjunctiva are very good places to grow
HSV virus. You also can also grow it from the blood, CSF.
As I said, if you have a vesicle there is high titer of virus in
those vesicles and virus grows rapidly, but you can also take
direct scraping specimens and get the answer in minutes.
There are quite specific - remember if your rapid test is
negative, still wait for your culture because depending on the
titer of virus these rapid tests may be negative.
Enteroviruses. Throat and rectum are the sites that you
usually grow the virus, but if you have a patient who has
neonatal enteroviral infection and has meningoencephalitis,
this CSF can yield the virus, or the amount of tissue, viral
isolation is appropriate.
Hepatitis B virus. You look for the presence of appropriate
antigens to confirm the diagnosis in the infant’s serum.
11
 Features Enhancing Susceptibility of
Premature Infants to Respiratory Infec-
tions

• Intrinsic/host Immaturity
• Decreased IgG levels in direct proportion to gestation
• Decreased opsonic capacity in proportion to decreased C3
and B levels
• Decreased PMN chemotaxis; early depletion of marrow
storage reserves
• Decreases lymphocyte motility or adherence
• Extrinsic/iatrogenic/Factors:
• Cutaneous barriers violated
• Indwelling intravascular devices
• Suppression of normal flora by antimicrobials
• Tracheal intubation
• Consequences of oxygen therapy
• Multiple exposures to pathogens

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Prevention and Control of Infection in
Premature, LBW Infants
• Surveillance for nosocomial infection: prompt recognition of
outbreaks; initiation of control measures
• Appropriate handwashing procedures are the single most
important aspect.
• Isolation procedures: based on mode of transmission
Prevention and control of infections in premature low birth
rate infants. If it is rotavirus season, or RSV season, and you
seem to have an outbreak you could even decide to close
your nursery to preadmissions while the outbreak is brought
under control.
Appropriate handwashing procedures are the single-most
important aspect of preventing infections, not only in low birth
rate preterm babies, but in immunocompromised patients.
Gloves are not a substitute for handwashing.
Isolation procedures. Among preemies who are less than 32
weeks gestation, almost one-half have BPD, and about one-
quarter are without BPD. Preemies less than 32 weeks
frequently require rehospitalization within a short period of
time.
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Re-hospitalization For Respiratory Ill-
ness in LBW Infants
• Among premature infants <32 wk gestation 45% with
bronchopulmonary dysplasia (BPD), require re-hospitaliza-
tion, and 25% without bronchopulmonary dysplasia (BPD),
require re-hospitalization
• Premature infants without BPD require re-hospitalization at
a rate 10-fold higher than term infants
• BPD infants are more likely to require multiple re-admissions
and prolonged stays than those without lung disease
• Infants discharged before RSV and influenza season (July-
Dec.) are significantly more likely to be readmitted than
infants discharged in other months
• Increased airway resistance and bronchial hyperreactivity
add to predisposition of BPD infants to viral (especially RSV)
and bacterial pneumonias
• Presumptive therapy is indicated for infections in infants with
BPD
Preemies without BPD require rehospitalization at 10-fold
higher rate than term infants because the risk of a baby less
than 37 weeks gestation is getting neonatal sepsis, inci-
dence is 10-fold higher than the risk of a term baby getting
neonatal sepsis, and If this risk persists, the immunologic
problems persist and, therefore, the attack rate persists. If
you have babies with BPD, they are much more likely to
require hospital readmissions, and they are much more likely
to require a full month stay than those without lung disease.
From July to December preemies are more likely to be ex-
posed to RSV during the RSV and other respiratory virus
season, and if you are exposed, you are more likely to be
readmitted. So the respiratory virus is responsible for this
seasonal distribution of readmissions.
Increased airway resistance and bronchial hyperactivity add
to the predisposition of bronchopulmonary dysplasia infants
to viral illnesses. Abnormal lung mechanics, abnormal im-
munity makes you more susceptible both to viral and bacte-
rial infections.
Presumptive therapy is indicated for infections in infants with
BPD.
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 Omphalitis
• Definition: Infection of the umbilicus
• Predisposing Features: LBW infant; complicated delivery
• Incidence: 2%
• Onset: Mean age 3 days
• Agents: S. aureus, group A streptococci, Bacteroides
Omphalitis. Omphalitis is infection of the umbilicus. It is
more common in low birth weight infants or in complicated
deliveries.
The mean age of onset is three days, and the pathogens that
we are thinking about are staph aureus, group A streptococ-
cus, bacteroids. Group A strep is on the list if the newborn
goes home because a sibling with impetigo, touches that
moist cord before it dry. Group A strep is very easily trans-
missible and very rapidly progressive, and so the infant will
present quite quickly.
15
 Funisitis
• Inflammation of the Umbilical Cord
• Agents
• Group A Streptococcus: wet, malodorous umbilical stump
with minimal inflammation
• Syphilis: "necrotizing funisitis," umbilical cord swollen,
discolored red, white and blue--resembling a barber's pole.
Involves matrix with perivascular inflammation and
obliterative endarteritis
• Candida: in association with congenital cutaneous disease
Funisitis is inflammation, not necessarily infection. You may
have inflammation of the umbilical cord from maternal
chorioamnionitis, for example, without the isolation of an
organism.
Syphilis could be a diagnostic possibility if you have the
placenta and the cord remaining. For the diagnosis of con-
genital syphilis, it can cause a necrotizing funisitis of the
umbilical cord, and the cord is swollen, and it has a barber
pole appearance (red, white, and blue). This involves matrix
perivascular inflammation and then endarteritis, so you see
this red, white, and blue thing. You see the red is the inflam-
mation, the white and the blue are manifestations in the
endoarteritis thrombosis, and lack blood flow to those partic-
ular areas.
16
 Omphalitis/funisitis
The diagnosis and therapy for omphalitis is culture of puru-
lent exudate, or subcutaneous aspirate. In the situation of
funisitis, you cut the cord. Histologic examination will show
the inflammation. Parenteral antibiotics are indicated in
• Diagnosis and Therapy
these particular situations most of the time.
• Culture from purulent exudate or subcutaneous aspirate
(differentiate from colonization) (omphalitis/funisitis)
• Histopathologic evaluation of cord (funisitis)
• Parenteral antibiotics and, for streptococcal funisitis,
topical treatment (triple dye or antibiotic)

17
 Ureaplasma Urealyticum
• Colonizes urogenital tract of ~50% of healthy adults
• Accounts for 20-30% of non-chlamydial NGU cases
• Associated with spontaneous abortion, chorioamnionitis and
fetal demise; causation?
• Vertical transmission rate during vaginal delivery is ~50%
• Colonizes the eyes, throat, umbilicus and perineum of
newborns; may persist for months
Ureaplasma urealyticum. Ureaplasma has one species that
is pathogenic for humans. Urealyticum was named because
this organism requires urea for its metabolic pathway. It
colonizes the urogenital tract in 50% of healthy adults, so it is
a very common colonizer in sexually active adults. It ac-
counts for 20% to 30% of nonchlamidial NGU cases. It is
associated with spontaneous abortion, chorioamnionitis and
fetal demise; but the organism may not necessarily be caus-
ing these events.
Vertical transmission during vaginal delivery occurs about
50%, so if your pregnancy population is colonized 50%, you
can know that about one in four babies might be colonized
with this organism. The colonization sites in the newborn are
the eyes, the throat, the umbilicus, and the perineum, and
this persists for many months. It may last six to twelve
months, then it goes away, and you do not see ureaplasma
again until the age of sexual activity, and then you go up to
50%.
18
 Ureaplasma Urealyticum in Newborn
Infants
• Associated causally with 'pneumonia' in some low birth
weight infants, but incidence and impact is uncertain
• Presence in tracheal aspirate cultures does not predict
respiratory deterioration in low birth weight, intubated infants
It is associated with a pneumonitis syndrome in the newborn
period. Most of these babies are low-birth weight, early
gestation infants, but the exact incidence is unknown, and
the impact of these lung abnormalities are unknown. If you
have somebody with radiographic lung disease and you grow
ureaplasma urealyticum from tracheal aspirate secretions,
erythromycin is the drug of choice here, just like with
Chlamydia, the optimal duration is ten days.
It has been isolated from the CSF of preterm infants with or
without cell inflammation signs in its spinal fluid, but its
pathological role is not clear at this time.

with lung disease

• It has been isolated from CSF of preterm infants; pathologic
role is unclear
• Isolation requires special transport media and urea-contain-
ing broth
• Erythromycin (25-40 mg/kg/day in 4 doses) for 10 days is
treatment of choice

19
 Escherichia Coli Meningitis
• Source usually is maternal but nosocomial acquisition is
possible
• Predisposing factors include maternal chorioamnionitis,
preterm delivery, and prolonged rupture of membranes
• 50% of cases have onset <7 days of age (3-7 most common)
• K1 capsular polysaccharide-containing strains: ~40% of
bacteremias, 75% of meningitis cases
E. coli meningitis. The source is maternal, like for other
forms of meningitis in the newborn and gram positive new-
born infection. With E. coli, nosocomial transmission is
possible. Usually we are talking about late onset acquisition
when we are talking about nosocomial acquisition. The
predisposing factors include the same kinds of maternal
factors that predispose patients to infection with other agents
besides E. coli, such as maternal chorioamnionitis. Preterm
delivery and prolonged rupture of membrane. Half of those
started in the first seven days of life. It was interesting that
there was a peak between age three and age seven, and
then a later peak of late onset disease.
20
 E. Coli Meningitis: Management
• Initial Therapy: ampicillin and gentamicin or ampicillin and
cefotaxime when gram-negative meningitis suspected
• Modify antimicrobial therapy based on susceptibility testing;
minimum duration 21 days
• Assess ventricular status early (head ultrasound or CT)
• Case-fatality rates (15-40%); neurologic sequelae mandate
careful audiologic and neurologic follow-up
Management of gram negative meningitis. Initial therapy is
ampicillin and gentamicin that you normally use for early
onset meningitis, and this is quite adequate initially, realizing
that some strains are going to be ampicillin resistant.
Ampicillin and cefotaxime, would be used, based on suscep-
tibility; 21 days of therapy is required. Some complicated
patients, especially those with ventricular illnesses are going
to require longer term therapy for cure.
Ventriculitis with obstruction must be determined early, and
the easiest way to do that is with a head ultrasound. If you
see ventricular dilatation then you can suspect there is a
block and you may need to assess the ventricular fluid as
part of your culture follow-up and efficacy of cure. If you have
ventriculitis, if the CSF is sterilized, ventricular fluid is persis-
tently positive, that is going to be a patient who is going to
relapse if you treat only 21 days and you need to treat longer.
The case fatality rates are still substantial. Case fatality is
15% to 20%.
21
 Listeriosis: Sources
Listeria in the perinatal period may be transplacental. This is
different than E. coli, this is different than group B strep, this
is something that can be transmitted transplacentally, or you
• Perinatal Period can see ascending intrapartum transmission like the more
typical neonatal pathogens. This may be going on for a very
• Transplacental or ascending intrauterine infection
long time at the time you see the baby. Exposure during
• Exposure during delivery delivery may also occur with Listeria, and the clinical syn-
dromes that you see with exposure during delivery are quite
• Environmental sources (late-onset disease) similar to the clinical syndrome with E. coli , sepsis and
group B strep sepsis. The distinctive feature of Listeria is the
ability to pass the placenta early on and cause quite a dis-
tinct transplacental syndrome. Pregnant women are also
vulnerable. Listeria colonization of the genital tract is uncom-
mon, but when it is there it may be associated with preterm
delivery and other obstetric complications. The most com-
mon one is chorioamnionitis. These women are quite ill.
They do fine with appropriate antimicrobial therapy, but they
have high fever, leukocytosis, and flu-like syndrome.
Food-borne Listeria has a variety of sources related to food.
Contaminated dairy products is the big one because Mexican
goat cheese is a favorite.

22
 Pregnant Women
• Maternal genital tract occurs in association with preterm
delivery and other obstetric complications (e.g. amnionitis)
• Food-borne
• Contaminated dairy products
• Undercooked poultry
• Prepared meats (pate, hot dogs)
• Cabbage contaminated with animal manure
Undercooked poultry, prepared meats such as paté, hot
dogs. Cabbage has been implicated in a number of salad
outbreaks of listeriosis. Remember that the mother may eat
these things and transmit the organism to the fetus.
When the baby develops listeriosis, the mother may say that
she has not been that ill but she has had some sort of a viral
illness. In more than half of the babies, an intrapartum history
of amnionitis is present.
23
 Listeria Monocytogenes Infections:
Patients with decreased cell mediated immunity are at risk
for listerial infections, and people who have decreased cell
Associations mediated immunity are at risk for listerial infections.

The one thing to remember is that healthy people with a

contaminated food exposure may become ill with Listeria,
• Maternal and occasionally present with high fever, flu-like symptoms
• Fecal or genital carriage and documentation of bacteremia or occasionally meningitis.

• Amnionitis
• Flu-like illness (fever, malaise, headache, myalgia)
• Infant
• Mother with symptomatic prodrome (65%) or amnionitis
• Decreased Cell-mediated Immunity
• Cancer chemotherapy; steroid therapy; congenital immuno-
deficiency; HIV disease; hepatic or renal disease
• Healthy Host
• Ingestion of contaminated food

24
 Listeriosis During Pregnancy
Listeriosis during pregnancy. In the first 16 weeks you may

illness. If you have somebody in July who has a flu-like ill-

• Infection (<16 wks) may cause abortion or stillbirth ness, you should be suspicious. If it’s a pregnant woman,

• Maternal influenza-like illness occurs 2-14 days before ery, and it may be precipitated by recurrence of fever at the
delivery; delivery is often precipitated by recurrence of fever time of delivery.

• Chorioamnionitis is frequent, favoring the transplacental route

of transmission
Maternal recovery is usually complete

25
 Features of Early-onset Listeriosis
group B streptococcus. These two syndromes have lots of
analogy in terms of age of onset, birth weight, obstetric
• Meconium staining (green or brown amniotic fluid), cyanosis,
usually a bacteremic illness early, and a meningeal focus
apnea, respiratory distress at delivery
late. Case fatality ratios are going to be significantly higher
• Common signs of infection: pneumonia (with hypoxia), sepsis,
meningitis (less common)
• Granulomatous rash with 1-2 mm microabscesses
(erythematous base) on skin and in pharynx
 Features of Late-onset Listeriosis
With the transplacental syndrome, you may see a

help with a diagnosis in addition to cultures. There seems to

• Onset 1-8 weeks of age (male predominance) be a male predominance. The age of onset goes into the

• Major form of infection is meningitis month. The major form of late onset infection is meningitis
Symptoms are not distinctive (fever, irritability, lethargy, poor and the symptoms are not distinct. These patients present

feeding) a diagnosis by doing a lumbar puncture.

3)
• CSF pleocytosis (150-3,000 WBC/mm early monocytic then
later, lymphocytic predominance

27
Listeriosis Beyond the Neonatal Period
Beyond the neonatal period, It may occur in the normal host,
and there are less common manifestations such as the
rhomboencephalitis, brain abscess, osteomyelitis, and
• Clinical Settings endocranitis.

• Renal transplantation, malignancy, HIV infection

• Usual Presentations
• Meningitis or sepsis
• Less Common Manifestations
• Rhomb encephalitis, brain abscess, arthritis, osteomyelitis,
endocarditis, endophthalmitis, peritonitis
• Infection in Normal Host
• Occurs, but rarely

28
 Treatment of Listeriosis
Ampicillin and penicillin are drugs of choice, but they are
inhibitory not cidal unless you combine them usually with
gentamicin (the combination is cidal). In the non-central
nervous system infections, most people use combination
• Ampicillin, penicillin, erythromycin, tetracycline are therapy initially, and complete therapy with ampicillin.
Ampicillin is usually preferred because it is more active and
bacteriostatic; in vitro. Cephalosporins are not active.

TMP-SMX, ampicillin appear bactericidal

• Recommended initial regimen: ampicillin and gentamicin
(combination is bactericidal); then ampicillin alone
• Penicillin-allergic patient: vancomycin and gentamicin or (for
non-perinatal infections) TMP-SMX
• Cephalosporins are not active against Listeria

29
Group B Streptococcus Vertical Trans-
mission and Infant Colonization

• Vertical transmission in 50% of infants born to GBS colonized

women (not given intrapartum penicillin)
• Neonatal colonization:
>24 hrs = rectum > throat > umbilicus
>30 days = rectum >throat
• Onset of sexual activity
Sites = gastrointestinal tract > genital > throat

30
Early- and Late-onset Neona-
tal GBS Infection

Feature Early-Onset Late-Onset

Mean age at 8 hr 27 days

onset

Incidence 13-3.7/1000 live 0.6-1.7/1000 live

births
births

Obstetric com- Common Unusual

plications

Manifestations Pneumonia (40%) Bacteremia

Bacteremia (45%) (50%)Meningitis
Meningitis (15%) (35%)

Serotypes All Type III predomi-

nates

Fatality rate 8-6% 2-10%

31
Optimal Methods and Sites for Recovery
of
GBS During Pregnancy

• Screening at 26-28 weeks gestation has PPV of 73% and

NPV at 92% for colonization status at delivery; at 35-37
weeks, these increase to 96% and 100%
• Swab of lower vagina and anorectum necessary to define
colonization
• Process culture in selective broth medium

32
 Treatment Regimens for Group B
Streptococcal Infections

Diagnosis Antibiotic Dose (per Duration

kg/d) (days)

Meningitis Ampicillin 300-400 Until CSF

+ mg sterile and
gentamicin 7.5 mg susceptibility
then then known; com-
penicillin G 400,000- plete 14-21
500,000 U

Bacteremia , Penicillin G 150,000- 10

soft tissue 200,000 U
infection
pneumonia

Septic arthri- Penicillin G 200,000 U 14-21

tis

Osteomyelitis Penicillin G 200,000 U 21-28

Endocarditis Penicillin G 300,000- >28

plus 400,00 U
gentamicin
for the
initial 7-14
days

33
 Intrapartum Chemoprophylaxis to
Prevent Early-onset GBS Infections

• Choice of obstetrical strategies: GBS culture-based or risk

factor-based
• Penicillin G IV (5 MU initially; 2.5 MU Q4h) until delivery
(alternatives = clindamycin or erythromycin)
• Timing: 4 hours (>2 doses) before delivery assures greatest
efficacy (Pylipow, Pediatrics 1994;98:631-5)

34
 References

Baker CJ, Edwards MS. Group B streptococcal infections. In:

Remington JS, Klein JO, editors. Infectious diseases of the fetus and
newborn infant. 4th ed. Philadelphia: W.B. Saunders Co., 1995;980-
1054.

Bortolussi R, Schlech WF III. Listeriosis. In: Remington JS, Klein JO,

editors. Infections diseases of the fetus and newborn infant. 4* ed.
Philadelphia: W.B. Saunders Co., 1995; 1055-1073.

Committee on Infectious Diseases. American Academy of Pediatrics.

Parvovirus, erythema infectiosum and pregnancy. Pediatrics
1990;85:131-133.

Committee on infectious diseases and committee on fetus and new-

born, AAP. Revised guidelines for prevention of early-onset group B
streptococcal (GBS) infection. Pediatrics 1997;99:489-496.

Cunningham CK, McMillan JA, Gross SJ. Rehospitalization for

respiratory illness in infants of less than 32 weeks gestation. Pediat-
rics 1991;88:527-532.

Da Silva O, Gredson D, Hammerberg O. Role of Ureaplasma

urealyticum and Chlamydia trachomatis in development of
bronchopulmonary dysplasia in very low birth weight infants. Pediatr
Infect Dis J 1997;16:364-369.

Glaser JH. Ureaplasma urealyticum. In: Long SS, Pickering LK,

Prober CG, editors. Principles and practice of pediatric infectious
diseases. New York: Churchill Livingstone, Inc., 1997; 1111-1114.

Klein JO, Remington JS. Current concepts of infections of the fetus

and newborn. In: Remington JS, Klein JO, editors. Infectious diseases
of the fetus and newborn infant. 4* ed. Philadelphia: W.B. Saunders
Co., 1995; 1-19.

Red Book of the American Academy of Pediatrics. Syphilis.

1997;504-514.

Risks associated with human parvovirus B-19 infection. MMWR

1989;38:81-97.

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