Management of Perinatal Infections Asid 2002 Rev 2007 PDF

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An infection during pregnancy that could

damage the fetus or infant is much less
common than suspicion or fear of infection.
Vague, nonspecific symptoms malaise,
aches and pains, headache, tiredness, nausea
- are the hallmarks of many vertically
transmissible maternal infections but they are
also common during pregnancy or in any
busy, stressful life. In pregnant women they
cant be dismissed as trivial as they may be in
others.
This publication represents a consensus
among specialists in perinatal infection. It has
been endorsed by the Australasian Society
for Infectious Diseases and the Royal College
of Obstetricians and Gynaecologists of
Australia and New Zealand. We hope it will
not discourage nonspecialists from referring
pregnant women with suspected infection
during pregnancy, but that it will help to guide
the initial assessment and investigation of the
patient, and prevent unnecessary anxiety or
hasty decisions.
Management of
Perinatal Infections
Cytomegalovirus
Enterovirus
Hepatitis B
Hepatitis C
Herpes Simplex Virus
Human Immunodeficiency Virus
Listeria
Mycobacterium Tuberculosis
Parvovirus
Rubella
Streptococcus - Group B
Toxoplasma
Treponema Pallidum (Syphilis)
Varicella Zoster Virus
Edited by Dr Pamela Palasanthiran,

Dr Mike Starr, and Dr Cheryl Jones
Introduction by Prof Lyn Gilbert
AUSTRALASIAN SOCIETY FOR
INFECTIOUS DISEASES 2002

Management of
Cytomegalovirus
Enterovirus
Hepatitis B
Hepatitis C
Listeria
Parvovirus
Rubella
Toxoplasma
Edited by Dr Pamela Palasanthiran, Dr

Mike Starr, and Dr Cheryl Jones

Copyright 2002 All rights reserved.

This book is copyright. Except as permitted under the Copyright Act 1968, (for example a
fair dealing for the purposes of study, research, criticism or review) no part of this book
may be reproduced, stored in a retrieval system, or transmitted in any form or by any
means without prior written permission. All inquiries should be made to Book House at the
address below.
ISBN 1 74018 222 7
Published by the Australasian Society for Infectious Diseases (ASID)
145 Macquarie Street, Sydney NSW 2000
Ph: (02) 9256 5475 Fax: (02) 9256 9692 e-mail: asid@racp.edu.au
www.racp.edu.au/asid
Reprinted in Australia 2005 by Wild & Woolley,
a division of Books & Writers Network Pty Ltd
Watsons Bay
2006:
Some updates and/or emendations have been included for selected algorithms under the
heading "Emendations". The comments are not comprehensive and are meant as added
information pending a new edition of this publication.
The Editors
C O N T E N T S
Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .iv
Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .v
Dr Pamela Palasanthiran, Dr Mike Starr, Dr Cheryl Jones
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .vii
Prof Lyn Gilbert
Cytomegalovirus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Dr Pamela Palasanthiran, Dr Cheryl Jones, Dr Sue Garland
Enterovirus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Dr Alison Kesson
Hepatitis B Virus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .9
Dr Jim Buttery
Hepatitis C Virus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13
Dr Jim Buttery
Herpes simplex Virus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16

Dr Cheryl Jones
Human immunodeficiency Virus . . . . . . . . . . . . . . . . . . . . . . . . . 19

Dr Pamela Palasanthiran
Listeria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24
Dr Lesley Voss
Mycobacterium tuberculosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27
Dr Mike Starr & Dr Allen Yung
Parvovirus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30
Prof Lyn Gilbert & Dr Mike Starr
Rubella . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33
Dr Clare Nourse
Streptococcus, group B . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36
A/Prof Suzanne M. Garland & Dr Mike Starr
Toxoplasma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39
Prof Lyn Gilbert
Treponema pallidum (Syphilis) . . . . . . . . . . . . . . . . . . . . . . . . . .42

Dr Andrew Daley & Prof Lyn Gilbert
Varicella zoster Virus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45

Dr Anne Marie Heuchan & Prof David Isaacs
References and Acknowledgements . . . . . . . . . . . . . . . . . . . . . . 51
iii
C O N T R I B U T O R S
Dr Jim Buttery, Paediatric Infectious Diseases, Physician, Royal Childrens

Hospital, Melbourne, Vic
Dr Andrew Daley, Clinical Microbiologist, Department of Microbiology and
Infectious Diseases, Womens and Childrens Health, Parkville, Vic
A/Prof Suzanne M. Garland, Director, Department of Microbiology & Infectious
Diseases, Womens and Childrens Health, Parkville, Vic
Prof Lyn Gilbert, Head, Centre for Infectious Diseases & Microbiology, Institute
of Clinical Pathology and Medical Research, Westmead Hospital, Sydney,
NSW
Dr Anne Marie Heuchan, Specialist Registrar in Neonatology, The Royal
Hospital for Sick Children, Glasgow, UK
Prof David Isaacs, Senior Staff Specialist, Department of Immunulogy and
Infectious Diseases, The Childrens Hospital at Westmead, NSW
Dr Cheryl Jones, Paediatric Infectious Diseases Consultant, The Childrens
Hospital at Westmead, NSW
Dr Alison Kesson, Medical Virologist, The Childrens Hospital at Westmead, NSW
Dr Clare Nourse, Paediatric Infectious Diseases Physician, Womens and
Childrens Health Service, Mater Hospital, Brisbane, Qld
Dr Pamela Palasanthiran, Staff Specialist, Paedriatric Infectious Diseases, Sydney
Childrens Hospital, Randwick, NSW
Dr Mike Starr, Paediatric Infectious Diseases Physician, Royal Childrens
Hospital, Melbourne, Vic
Dr Lesley Voss, Paediatric Infectious Diseases Physician, Starship Children's
Hospital, Auckland, NZ
Dr Allen Yung, Infectious Diseases Physician, Victorian Infectious Diseases
Service, Melbourne, Vic
iv
F O R E W O R D
This comprehensive set of contemporary algorithms on the

management of perinatal infections has been written by a team of
Australian and New Zealand paediatric infectious disease experts who
are all members of the Australasian Society of Infectious Diseases
(ASID).
The impetus behind this project was the recognition that simple
guidelines are needed for general practitioners, obstetricians and
paediatricians to address common issues once an infectious agent
complicates a pregnancy. Questions such as Do I really have this
infection? Can it be treated during my pregnancy? Will I pass it on to
my baby? and What will happen if I do? frequently arise. Thus, the
algorithms follow 4 themes (where possible): antenatal diagnosis of
the infectious agent, antenatal management, perinatal transmission
risks, intervention strategies if available, and management of the
newborn. It is stressed that these algorithms are evidence-based
where possible but in many cases, represent consensus
recommendations and are intended only as a set of guidelines.
We acknowledge the contributions of Drs. Sonia Grover and Ted
Weaver who reviewed the final versions of these algorithms and
provided invaluable feedback on behalf of the Royal Australian and
New Zealand College of Obstetricians and Gynaecologists
(RANZCOG) and members of ASID who provided comments and
feedback on early drafts. We also wish to thank ASID and in
particular the ASID council for funding for this project.
Above all, we acknowledge the authors for the invaluable time they
have contributed to this project, on top of their primary work
commitments. We also thank Professor Lyn Gilbert for her
encouragement and unfailing guidance. Their combined support has
been a significant force behind this achievement
We hope these algorithms will be as useful to you as they have been
for us.
Pamela Palasanthiran
Mike Starr
Cheryl Jones
March 2002
I N T R O D U C T I O N
An infection during pregnancy that could damage the fetus or infant is

much less common than suspicion or fear of infection. Vague,
nonspecific symptoms malaise, aches and pains, headache,
tiredness, nausea are the hallmarks of many vertically transmissible
maternal infections but they are also common during pregnancy or in
any busy, stressful life. In pregnant women they cant be dismissed as
trivial as they may be in others. Laboratory tests may provide the
answer but can be hard to interpret. On the other hand, vertically
transmissible infections are often asymptomatic. Routine antenatal
screening is recommended for some on the basis of criteria including:
Incidence of maternal infection, transmission to the fetus and
damage if infection occurs.
Availability of a reliable screening test
Availability of a safe effective intervention to prevent fetal/infant
infection and reduce damage.
Sometimes asymptomatic women are screened for infections other
than those recommended. An unexpectedly positive result then
creates a problem that must be managed. It can be difficult to
determine the predictive value of a positive test, in the absence of
symptoms. The result may not indicate current or recent infection, but
this may become apparent only after additional serological testing
and/or examination of amniotic fluid. Meanwhile, it will have caused
anxiety to the patient and her family. Her medical adviser will be
worried, not only for the wellbeing of the patient and her fetus, but also
about the potential for litigation if things go wrong. If the results remain
uncertain as they often do the patient may choose to terminate her
pregnancy because she cannot tolerate even a small risk of having an
abnormal infant. On the other hand, even an inappropriate screening
test will sometimes detect a significant infection and the potential to
intervene and prevent an unfortunate outcome.
Negotiating this minefield of psychological, medicolegal, ethical and
medical dilemmas is difficult enough for the specialist with a particular
interest in infections in pregnancy. But for the average GP or
obstetrician, for whom they are rare complications, it can be nervewracking. These algorithms outline recommended antenatal screening
tests, how to manage symptomatic infection or a positive screening
test and the range of tests available to assist in risk assessment.
vii
There are a few common themes:

Significant decisions about management of a suspected infection
during pregnancy should never be based on the result of single
test. The test should always be repeated, preferably by a different
method and on another specimen of serum. False positive IgM
results are not uncommon and, even in the best laboratories, sera
occasionally get mixed up.
Laboratories are advised to keep serum, sent for routine antenatal
screening, for at least 12 months. If the possibility of infection arises
later it can be retrieved and tested in parallel with a later specimen,
to show or exclude seroconversion, which is much better evidence
of recent infection than IgM.
If only a single serum is available or the results do not change in
serial samples, measuring IgG avidity (a measure of maturity of the
IgG response, which develops over a period of several months)
can help. A high avidity can exclude recent infection, even in the
presence of persisting IgM. The reverse is not necessarily true low avidity does not always imply recent infection.
This publication represents a consensus among specialists in perinatal infection. Its completion is a major achievement for the editors,
Pamela Palasanthiran, Mike Starr and Cheryl Jones. It has been
endorsed by the Australasian Society for Infectious Diseases and the
Royal College of Obstetricians and Gynaecologists of Australia and
New Zealand. We hope it will not discourage nonspecialists from
referring pregnant women with suspected infection during pregnancy,
but that it will help to guide the initial assessment and investigation of
the patient, and prevent unnecessary anxiety or hasty decisions.
Lyn Gilbert
Centre for Infectious Diseases and
Microbiology
Institute of Clinical Pathology and
Medical Research
Westmead Hospital
March 2002
viii
C Y T O M E G A L O V I R U S
A L G O R I T H M
Diagnosis of Suspected Maternal CMV Infection

Possible indications for antenatal testing
Routine antenatal testing?a
History suggestive of CMV illnessb
Exposure to known CMV infected
individual or blood product
Immunocompromised
Abnormalities on routine antenatal
ultrasound (SEE ALGORITHM 2)
LABORATORY
INVESTIGATIONS1
DIRECT VIRUS DETECTION
SEROLOGYc
IgG ve
IgM ve
IgG +ve
IgM ve
NOT CMV INFECTION

but susceptibled
PAST
INFECTION
IgG ve or +ve
IgM +vec
CMV direct
flourescent
antibody
(DFA)
No change
in IgG
Possible
recent
infection
CMV specific
IgG avidityc
Low probable
recent infection
High probable
past infection
RECENT PRIMARY INFECTION

NOTES
a As CMV is the leading cause of congenital
infections
(0.3 2% of live births), antenatal testing
remains a consideration, especially in
counselling issues for primary maternal
CMV infections. If done, there should be
appropriate management plans.
All pregnant women should be advised
about simple infection control
precautions to reduce transmission risk
eg handwashing after nappy changes
and contact with respiratory tract
secretions, especially with children
<2 years of age attending day care
Some groups identified at higher risk of
primary CMV as determined by annual
Nucleic Acid
Detection
PCR (DNA),
NASBA (RNA)
COMMENTS: Relevant samples include buffy coat (white

cells), nasopharyngeal aspirate or saliva and urine
1. Sensitivity for detecting infection:
DFA = 8090%, while PCR = 95100%
2. Sensitivity for detecting disease:
DFA = 7080% compared with PCR = 5090%
3. Specificity for disease: DFA = 95-100%,
virus isolation = 95100% and PCR = 4050%
4. Time to results: DFA and PCR: "rapid";
Virus isolation could take up to 4 weeks
Repeat test 2-4 weeks later
Seroconversion
or rise in IgG
CMV isolation
SEE ALGORITHM 2
+ve
seroconversion rates
specificity). More sensitive assays can
I. Day care workers 11% per annum
detect IgM in 5% for up to 2 years
II. Parents with child in day care 2030%
IgM can persist for months after primary
per annum
infection or reappear with reactivation or
In comparison, healthcare workers
re-infection
seroconvert at a rate comparable to the
False positive IgM occur with crossgeneral population ie 23% per annum
reactivity with other herpes viruses,
b Most primary CMV infections are
pregnancy or autoimmune disorders
asymptomatic. Suspect primary CMV
CMV IgG avidity assay is reported to be
disease in a viral illness associated with
a reliable indicator of primary infection.
atypical lymphocytosis which is "Monospot"
Low avidity = probable recent infection,
negative (also seen in primary
with progression to high avidity with
toxoplasmosis) or with clinical syndromes
time2
associated with CMV disease
d If still concerned or if serology taken within
c Overall, IgM is ~75% sensitive by ELISA
2 weeks of clinical illness, repeat in 2
Commercially available assays: IgM
weeks
results may lack specificity (~75%
A L G O R I T H M
Management of
Primary Maternal CMV Infection
CONFIRMED PRIMARY MATERNAL CMV
Fetal Diagnosis
Fetal Risk Assessment

SEE ALGORITHM 3
Therapy
Supportive
None available for either
prevention of transmission or
for effective treatment of
congenital CMV
Serial Fetal
Ultrasoundsa
Invasive in utero
Investigationsb
AMNIOCENTESIS
PCR
FETAL BLOOD SAMPLING
Culture
FBE (Plt)
LFT
Serology
(IgM)
PCR
<20 w
>20 w
<20 w
>20 w
>20 w (Not performed under 21 weeks)
45%
80100%
18%
56%
5080%
Sensitivity of Test
NOTES
a. Features associated with symptomatic congenital CMV infection include:
hydrocephalus (ventricular dilation)
microcephaly
ascites
intrauterine growth retardation (IUGR)
hydrops fetalis
pleural or pericardial effusions
oligo or polyhydramnios intracranial calcification
hepatomegaly
abdominal calcification
pseudomeconium ileus
Caution advised in interpretation of findings as presence of signs not
always predictive of degree of fetal damage. The sensitivity of fetal ultrasound is hard to evaluate from the literature. Overall, ? 3050% sensitive.
b. Invasive in utero investigations35
Techniques available but all lack sensitivity. Experience with fetal blood
sampling is limited.
Diagnosis is best achieved by a combination of fetal ultrasound +
amniocentesis (for PCR) +/- fetal serology

Diagnosis by amniocentesis testing (PCR & culture)
and fetal IgM is about 45% sensitive overall if taken <
20 weeks and 80100% sensitive if taken > 20 weeks
gestation. Specificity approaches 100%
Sensitivity is increased by waiting 6 weeks after
maternal infection
Positive results do NOT predict any degree of fetal
damage
Quantitative PCR and/or culture may identify infected
fetuses at risk of symptomatic disease (direct relationship between high load and risk)6
Further data required before active recommendation.
Positive results: pregnancy termination is an option
by informed choice.
A L G O R I T H M
Congenital CMV:
Fetal Risk Assessment
PRIMARYa
NON-PRIMARY
(reinfection or reactivation)
50% risk of transmissionb
1% risk of transmission
Symptomatic
congenital CMV 10%
Risk of
sequelae
90%d
Normal
10%
Asymptomatic
congenital CMV 90%
Risk of
sequelae
10%e
Symptomatic
congenital CMV 1%c
Asymptomatic
congenital CMV 99%
RISK OF SEQUELAE up to 10% e
Normal
90%
Risk of fetal morbidity overall is 2025% SEE ALGORITHM 4
NOTES
a. Australian epidemiology: The incidence of primary CMV infection in pregnancy in Australia is estimated to be 6/1000 pregnancies.
The incidence of congenital CMV is estimated to be 0.3 to 0.6%7
b. The risk of transmission is distributed equally between the 3 trimesters. However,
Risk of severe adverse neurological outcome more likely in 1 infection in first half of pregnancy. Features of fetus affected in early
infancy include small for gestational age (SGA), microcephaly and intracranial calcifications
A fetus affected late in pregnancy is more likely to have acute visceral disease (hepatitis, pneumonia, purpura and severe
thrombocytopenia)
c. Infection of CMV-seropositive women with a different CMV strain can lead to intrauterine transmission and symptomatic congenital
infection.8
d. Main concerns of symptomatic congenital CMV infection are:
1. A mortality rate of between 1030%
2. Neurological sequelae of microcephaly (3550%), seizures (10%), chorioretinitis (1020%), mental retardation (70%)
3. Sensory neural hearing loss (SNHL, 2550%)9
30% )
Unilateral
Bilateral
70% ) Progressive
57% (over 2 to 6 years?)
43% )
Stable
e. Main concerns of asymptomatic congenital CMV are
1.
Sensory neural hearing loss (5%)
Unilateral
64% )
Bilateral
36% ) Progressive
36% (over 2 to 6 years?)
64% )
Stable
If hearing is preserved at age 12 months, intellectual development is unlikely to be affected10
2. Chorioretinitis (2%)11
Emendation 2006
Algorithm 3: Congenital CMV: Fetal risk assessment
Prior maternal CMV immunity (i.e. seropositivity) results in an approximate
70% reduction in the risk of congenital CMV infection.E1 However, it has now
been demonstrated that the risk of congenital CMV infection after primary
maternal CMV infection remains elevated for up to four years postseroconversion, with the highest risk being in the first two years post
seroconversion. The overall risk is 12.7% post seroconversion, that decreases
to the baseline 1% risk by about 4 years post seroconversion.E2 The time of
seroconversion is usually unknown, however, this information may be helpful
when counselling a women of a child with congenital CMV infection about
the time of a subsequent pregnancy
A L G O R I T H M
Management of the
Newborn at Risk of Congenital CMV
Thorough physical examination at birtha
Ophthalmology
Radiological
Examination
Head ultrasound
hydrocephalus
(insensitive
investigation
for intracranial
calcification)
+ve
Laboratory Investigations
Must be done 3 weeks of birth
CT of brain
(+/-MRI)
intracranial
calcification
ventriculomegaly
cerebral atrophy
Serology
CMV IgM
ve
+ve
+ve
PCR
buffy coat
(white cells)
Viral culture
Urine
+/- NPA
ve
ve
+ve
+ve
Congenital CMV
SYMPTOMATIC
Intensity of management dependent
on extent of organ involvement
NOTES
a. Features of (typical) symptomatic congenital CMV
1. Neurological: (see text box, Algorithm 3)
2. Non-neurological: SGA (50%), petechiae/purpura
(5075%), hepatosplenomegaly (4060%), neonatal jaundice (4065%), pneumonia (<1%), dental
abnormalities (30%), inguinal hernias (males),
infant mortality (1030%).
3. Laboratory abnormalities: hemolytic anemia (1050%), platelets 75,000/mm (50%), direct hyperbilirubinemia 3 mg/dL (3570%), AST > 100 IU/L
(2580%), CSF protein >120 mg/dL (4550%)
4. Risk of serious bacterial infection (5%)
ASYMPTOMATIC
36 monthly review for first 2 years
including neurodevelopmental assessment
NOTES
1. Other baseline tests at birth: FBE & differential and LFT
2. Hearing tests: due to improved prognosis for speech development if hearing
abnormality detected early, suggest testing before 6 months, then annually
for the first 2 years of life, then close review till age 6 years if no problems
detected
3. All CMV-infected infants should have fundoscopy for retinal lesions and visual assessment by ophthalmologist at diagnosis. If abnormalities detected,
annual review recommended. Otherwise, monitor vision during infancy with
formal review if abnormalities detected.
4. Treatment options: nil. Ganciclovir (IV) for retarding the progress of hearing
loss in CNS disease associated with congenital CMV has been studied, but
follow-up data yet to confirm efficacy12
5. Congenitally infected babies are high CMV shedders. Pregnant health care
workers should be aware of this and infection control practices e.g., handwashing emphasised.
Emendation 2006
Algorithm 4: Management of the newborn
A randomised, controlled trial on intravenous ganciclovir therapy (for 6
weeks) in newborns with symptomatic congenital CMV and CNS disease
showed normal or improved hearing at 6 months (results did not reach
significance) and no hearing deterioration at 1 year (highly significant).
However, the high loss to follow-up (~ 60%) makes the clinical significance of
the data difficult to interpret and 63% had significant neutropenia. Therefore,
the potential side effects and social cost of 6 weeks of intravenous ganciclovir
therapy in an individual child must be weighed against a possible, but yet
unproven long term gain with this treatment.E3 There is currently no indication
for systemic antiviral therapy for infants without clinical signs of CMV
infection at birth (i.e. asymptomatic infection).
E N T E R O V I R U S
A L G O R I T H M
Antenatal Diagnosis of
Maternal Enteroviral Infections
If concerns raised about whether pregnant
woman has an enteroviral infection, are there
features consistent with enterovirus infection?
No
Yes
Observe mother and infant after birth
If there are clinical concerns, the diagnosis can

be made via serology, viral culture (nasopharynx
or throat swab & faeces) and/or PCR
SYMPTOMS OF ENTEROVIRAL DISEASE INCLUDE*:
DIAGNOSIS
Asymptomatic
Serology very insensitive, very specific

Viral culture varying sensitivity and specificity
PCR variable sensitivity
Fever
GIT symptoms eg diarrhoea
Encephalitis
INTERPRETATION OF RESULTS
Flaccid paralysis
Serology:
If the results are positive indicates infection;
if the results are negative infection is not
excluded due to poor sensitivity.
Herpangina
Hand-foot and mouth syndrome
Lymphonodular pharyngitis
Exanthem
Viral Culture:
Sensitivity varies depending on the sample.
Culture has high specificity but due to
prolonged shedding in faeces a viral culture
may be a "false positive" and not indicate a
current enteroviral infection.
Epidemic conjunctivitis
Myositis
Guillain-Barre syndrome
Mononucleosis-like syndrome
Pleurodynia
Acute haemorrhagic conjunctivitis
PCR:
Sensitivity and specificity are good.
Myocardidits
* peak incidence in the Spring/Summer months in non-tropical or temperate regions of Australia
NOTES
Enteroviral infections generally cause insignificant
illness, and perinatal transmission of enteroviruses
leading to significant symptomatic disease in infants is
rare. The literature on this is not comprehensive. Hence,
these algorithms are based largely on anecdotal
evidence and represent broad guidelines.
To date, there are no data on indicators of perinatal
transmission risks nor predictors of fetal or infant
damage.
A L G O R I T H M
Management of
Proven Maternal Infection
Pregnant or postnatal woman has
symptoms and signs consistent with
enteroviral infection which may be
supported by laboratory data
Woman has
mild disease
Woman has
severe disease
Symptomatic
therapy
Consider therapy
with pleconaril
Intrauterine, perinatal and

post-natal transmission occur
No reliable information
about correlates of risk of perinatal
transmission nor predictors
of fetal/infant damage
A L G O R I T H M
Antenatal Management
and Prevention Strategies
Management of
infected mother
Symptomatic
treatment of mother
Counselling
Prevention strategies possible

either before or during
pregnancy, labour or at birth
Polio vaccination prevents
polio. Good personal hygiene
to prevent faecal-oral
transmission especially if in
contact with a source case.
Enteric precautions apply if
patients are admitted.
Interpret clinical and

pathological Information
Risk assessment of fetal
Infection or abnormality:
there are no reliable risk data
Management of
antenatal care
The following has been reported:
abortion, congenital abnormalities,
stillbirth, symptomatic infant,
normal infant
A L G O R I T H M
Diagnosis, Management and Follow-up

of At-Risk Infants
Symptoms and signs of an infected infant
Asymptomatic, Febrile illness,
Sepsis-like illness, Respiratory illness
Herpangina, Coryza, Pharyngitis,
Laryngo-tracheo-bronchitis and bronchitis
Pneumonia, Vomiting and diarrhoea,
Hepatitis, Pancreatitis, Myocarditis
Examthem, Meningitis and encephalitis, SIDS
Diagnosis
Serology, viral culture and PCR
Treatment
Supportive care, polio vaccine,
IVIG may be of benefit if <6 weeks preterm
but no supporting data
Pleconaril limited data available5,6
Counsel mother
Prophylaxis
NOTES
Improved survival in small case
series of severe neonatal Ev
sepsis. Data group was too
small to determine if outcome
was significant. No activity
against Ev 71.5
Recommended neonatal dose
is 5mg/kg given orally every 8
hours. Bioavailability in
neonates is satisfactory.6
Nursery epidemics have been controlled

by infection control using enteric
precautions and prophylactic IVIG.
Follow-up
As clinically indicated by nature
and severity of infection
Emendation 2006
Enterovirus- Algorithm 4: A double blind placebo-controlled trial of oral
Pleconaril in 21 infants with enteroviral meningitis demonstrated plasma levels
sufficient for in vitro inhibition of enterovirus replication.E4 However, oral
Pleconoril has since been withdrawn from the market.
H E P A T I T I S
A L G O R I T H M
V I R U S
1
Antenatal Diagnosis of Hepatitis B

Routine screening recommended
Hepatitis B surface Antigen (HBsAg)
All HepBsAg positive

women require medical
referral post delivery
by midwife/doctor
managing pregnancy
HBsAg +ve
HBsAg ve
Confirm HBsAg+
Further serology
HBeAg
anti-HBeAb
LFTs
Not infected
Nil further action unless
high risk groupa
(offer mother vaccination
after delivery)
HBeAg+ve
High risk carrier
Ensure screening
+/- vaccination of
family members
HBeAg ve
LFTs abnormal
LFTs normal
Consider HBV DNA hybridisation

to detect pre-core mutants. (Available in reference
laboratories only. Turnaround time is slow.)
NOTES
a. High risk groups1
from area of high prevalence
household contact HB carrier
multiple sexual partners
IV drug use
tattoos/body piercing
DNA not
detected
DNA
detected
Low risk
carrier
High risk
carrier
H E P A T I T I S
A L G O R I T H M
V I R U S
2
Management of Hepatitis B in Pregnancy

Acute Hepatitis B
Chronic Hepatitis B infection (HepBsAg+)
SEE ALGORITHM 1
Trimester 1 and 2
perinatal transmission risk ~10%2
Late Pregnancy
perinatal transmission risk ~75% 2
Refer for supportive medical management

No demonstrated role for antenatal HBIG in
reducing subsequent perinatal transmission
Lamivudine (3TC) and -IFN
contra-indicated in pregnancy
Delivery:
no data regarding mode of delivery in
acute hepatitis
Caesarean section lowers risk of perinatal
transmission in chronically infected
HepBeAg positive mothers3
Baby:
HBIG and HB vaccine at birth
further HB vaccine at 2,4 & 12 months
(multivalent vaccines after first dose)5
arrange follow-up serology at 12 months
(SEE ALGORITHM 4)
NOTE
Current prospective data does not support an
increased risk of vertical transmission of Hep B after
amniocentesis.4
10
H E P A T I T I S
V I R U S
A L G O R I T H M
Hepatitis B: Exposure During Pregnancy

No Immunisation
Prior Immunisation
Check serology urgently
antiHBs > 10 mIU/mL
HBsAg neg
HBsAg pos
Nil
further
action
Check
HBeAg
status
SEE
ALGORITHM
4
HB vaccine to baby at
0,2,4 & 12 months if
ongoing risk exposure
(multivalent vaccines
after 1st dose)5
antiHBs < 10 mIU/mL
antiHBs > 10 mIU/mL
antiHBs < 10 mIU/mL
HB vaccine
HBIG within 72h if
high risk exposure
Nil further action
HB vaccine at 12
and 6 months5
HBIG within 72h if
high risk exposure
HB vaccine at 12
and 6 months5
Follow-up mother in
3 months: HepBsAg
Follow-up mother in
3 months:
HepBsAg HB vaccine
to baby at birth
HB vaccine to baby at
0,2,4 & 12 months if
ongoing risk exposure
(multivalent vaccines
after 1st dose)5
NOTES
Maternal risk of infection by mode of exposure:
needlestick: if donor eAg+ high risk 20-40%6
sexual contact
mucosal exposure
11
H E P A T I T I S
A L G O R I T H M
V I R U S
4
Management of Infants
of Mothers with Hepatitis B
Maternal serology:
HBsAg positive or
HBeAg positive or
HBV PCR positive
Delivery:
HepBeAg+ mothers: there is no evidence that Caesarean
section offers an additional advantage over the recommended
neonatal reg imen of Ig + vaccine in preventing ver tical
transmissions. A benefit was seen in one study where vaccine
only was used3
HBIG 0.5 mL IM
HB vaccine 0.5 mL IM
At birth: HBIG and HB

vaccine preferably within 12
hours5
Risk vertical transmission:

mother sAg+, eAg- 520%7,8
mother sAg+, eAg+ 7090% 9
90% infected infants become
chronic carriers6
At 2, 4 and 12 months:
HB vaccine
(multivalent schedule)
Breastfeeding:
HBV DNA and HBsAg
detected in breast milk10
no added transmission risk
demonstrated11
Follow-up serology at
12 months including HBsAg
HBsAg negative
HBsAg positive
No
further action
LFTs, HBeAg
Refer for ongoing
management
12
Emendation 2006
HEPATITIS B
Management of a mother exposed to HB during pregnancy (see Algorithm 3).

If maternal antiHBs titre < 10mIU/ml, give mother HBIG (400 IU, IM) as
soon as possible but within 72 hours of exposure. Also, give the mother HB
vaccine within 7 days of exposure and at 1 and 6 months post initial dose.E5
Management of an infant born to a HB carrier mother (see Algorithms 2 & 4):

e.g. mother with acute HBV in pregnancy or is HB antigen or PCR +ve. Give
HBIG (100 IU, IM) to the infant preferably within 12 hours of delivery
(efficacy markedly reduced if administration delayed beyond 48 hours after
birth). Monovalent HB vaccine should be given at the same time (other limb)
if possible, but do not delay beyond 7 days of life. Complete schedule with 3
more doses at 2, 4 and 6 or 12 months (timing dependent on combination
vaccine used). E5
Revised recommendation for primary HB vaccine schedule for babies

(Algorithm 3): when the risk of perinatal HBV transmission is low, the routine
Australian schedule is recommended i.e. birth (monovalent HB vaccine), then
combination vaccines at 2, 4 and 6 or 12 months (timing dependent on
combination vaccine used). E5
H E P A T I T I S
A L G O R I T H M
V I R U S
1
Antenatal Diagnosis of Hepatitis C

Known Hep C Ab +ve
All positive Hep C ELISA

tests need confirmation by
RIBA (recombinant
immunoblot assay) assay
on same sample
Confirm Hep C Ab +ve
All HIV +ve mothers need

Hep C RNA PCR irrespective
of Ab status as serology can
be falsely ve
Status unknown: Indications

for antenatal testing2
IV drug user (past or present)
known abnormal LFTs
previous blood products
before 1990
previous organ transplant or
haemodialysis
partner Hep C positive*
history of incarceration
Counsel re testing for:

Hepatitis B & HIV
Notifiable disease (coded)
Pre-test counselling
Hep C Ab +ve
Counselling
LFTs
Hep C RNA PCR
Hep C RNA PCR ve
Hep C RNA PCR +ve
Low risk carrier1
Demonstrated risk of
vertical transmission1
Refer for medical management

See ALGORITHM 2
Recommend postnatal Hepatitis A vaccination
13
Hep C Ab ve
*partner Hep C positive less

clear risk factor3
nucleotide sequence
homology seen in partners
negligible transmission in
sex-partner studies
Hep C transmission lower
than other sexually
transmitted diseases in high
risk groups
H E P A T I T I S
A L G O R I T H M
V I R U S
2
Management of Hepatitis C in Pregnancy

Hep C Ab +ve
Hep C RNA PCR

LFTs
Refer for management and counselling
HIV and Hepatitis B testing

after counselling
Hep C RNA PCR -ve
Hep C RNA PCR +ve
HIV/Hep C co-infection
Perinatal transmission risk

~0%4
Perinatal transmission risk ~6%4

Risk proportional to RNA load4
Perinatal transmission risk

Hep C 9-45%4
Delivery: no clear evidence re

mode of delivery and reduction
of perinatal transmisison
Breastfeeding: no increased risk

of transmission demonstrated
Interferon-alpha and
ribavirin therapy contraindicated in pregnancy
See ALGORITHM 3
14
H E P A T I T I S
V I R U S
A L G O R I T H M
Management and Follow-up of

Infants of Hepatitis C Infected Mothers
Birth
ensure hepatitis B immunisation within 24 hrs
check maternal records re HBV and HIV testing
Breastfeeding: not discouraged

transmission has not been documented5
Hep C RNA has been detected in breast milk 6
consider expressing and discarding milk if nipples
cracked or bleeding5
consider avoiding breast feeding if symptomatic
liver disease7
Follow-up:
anti Hep C Ab at 1218 months*
or if concerned earlier
anti Hep C Ab
Hep C RNA PCR
Anti Hep C Ab +ve

Infected child*
Anti Hep C Ab ve
Not infected
Hep C RNA PCR

LFTs
Hep C RNA PCR ve
Hep C RNA PCR +ve
Repeat serology
in 3 months
Refer for ongoing

management to
paediatric hepatologist:
repeat LFTs and HCV
RNA PCR
possible therapy
NOTES
Most uninfected infants are antibody negative by 12
months. If positive serology at 12 months, retest in 3
months before considering them infected. A small
percentage of perinatally infected children may clear
the virus1,4,8
15
Emendation 2006
HEPATITIS C
Algorithm 3 : Follow-up of infants of hepatitis C infected mothers E6
The general recommendation for testing a well child with perinatal HCV
exposure is to test the child for HCV antibodies at 18 months of age as
transplacental maternal HCV antibodies should clear by then.
When follow up cannot be guaranteed however, testing by HCV RNA PCR
(include LFT) should be performed earlier, but not at less that one month of age
as the sensitivity of HCV RNA PCR is 22 % at < 1 month of age. A single
positive PCR result after 1 month of age gives a post-test probability of infection
of 73% for a child born to an HIVve/HCV+ve woman, and 90% for a child
born to an HIV+ve/HCV+ve woman.E7 A positive or negative PCR result should
be confirmed on a separate occasion.E8 Negative PCR results but positive anti
HCV antibody in a child < 18 months of age usually suggests that the child is
not infected.8 However, HCV antibody (with accompanying liver function tests)
should be retested at or beyond 18 months of age to confirm this, as occasionally
it represents infection of the child in the absence of HCV viremia. E6, E 8
H E R P E S
S I M P L E X
A L G O R I T H M
V I R U S
Herpes Simplex Virus Infections in Pregnancy:

Risk Assessment of Neonatal Disease
YES
Maternal history of prior

genital HSV infection?
Symptomatic
prior infection
Asymptomatic
prior infection
Genital HSV (1 or 2) diagnosed during pregnancy

HSV culture type & serology determined
Recurrent
infection
(HSV Ab +ve
= HSV type from
genital culture)
Delivered
through a birth
canal with overt
vesicles (Only
20% are culture
positive)1
Overall risk
of neonatal
HSV disease
1%3
NO
No
prior infection
First genital HSV (1 or 2) diagnosed during pregnancy

HSV culture type & serology determined
New
acquisition
of other
HSV type in
genital area
"Initial nonprimary" infection

(HSV Ab -ve to
type cultured
from genital area
& HSV Ab +ve to
other type)
"Primary"
infection (HSV Ab
-ve to both types
+ HSV genital
culture +ve)
Seroconversion well before delivery

(ie prior to 3034 weeks)4
Delivered through a
birth canal with normal
appearance: (Risk of
shedding 1.4%.1 If shedding,
risk of transmission
is 3%, if not it is 0.02%2)
0.023%2
YES (Risk of
shedding 7%)4
NO
(or unknown)
3%4
30-50%1,4
Effect of Caesarean delivery on neonatal attack rate unknown3

NOTES
Most genital HSV infections (primary, non-primary or recurrent) are asymptomatic. ie most mothers of infants with neonatal HSV disease
were previously unaware of their own infection.
HSV-1 genital infection is being increasingly recognised- but is less likely to recur than genital HSV-2.
85% of neonatal HSV infections are acquired perinatally. True intrauterine infection accounts for 5% of reported cases, usually to
women with newly acquired infection. Spontaneous abortion, IUGR, preterm labour have also been reported. These complications are
rare (<1%) for women with primary or recurrent disease.4
16
H E R P E S
S I M P L E X
A L G O R I T H M
V I R U S
Maternal Management of Genital Herpes

Simplex Virus Infections in Pregnancy
History of genital HSV
(laboratory confirmed)
No prior history
of genital HSV
Serial genital cultures not predictive

of shedding during labour,
so are not recommended4
Consider use of suppressive

aciclovir (400 mg tds po) in women
with multiple recurrent overt lesions
First genital HSV infection

diagnosed during pregnancy
Recurrent
infection
(HSV Ab
+ve to type
from genital
culture
First genital
HSV infection
diagnosed
during labour
Obtain HSV serology (type

specific) + type genital culture
New infection (HSV Ab ve

to type from genital culture
In labour:
careful speculum examination
No
active
lesions seen
Proceed
to vaginal
delivery
Fetal scalp
electrode,
forceps,
& vacuum
delivery not
recomended
Management of
newborn as per
ALGORITHM 3
Active
lesions seen
(see notes)
ROM
>6
hours5
ROM
<6
hours5
Diagnosis made early

in pregnancy (1st or
2nd trimester) Counsel
as for ALGORITHM 1
Diagnosis made late

in pregnancy
(ie 3rd trimester)
Seroconversion well
before delivery (ie prior
to 30-34 weeks)4
Consider
suppresssive aciclovir
(400 mg po tds)6
Yes
No or
unknown
Deliver by Caesarean section

Perform genital "sweep culture." If vaginal delivery unavoidable:
fetal scalp electrode, forceps, & vacuum delivery not recommended
NOTES
Insufficient data are available on the effect of suppressive aciclovir on transmission to the newborn for either active recurrent or primary
genital maternal disease.
Careful speculum examination for active genital HSV should be performed on all women at delivery.
ROM>6 hours has been observed in one small study to increase risk of neonatal infection.5 However the efficacy of Caesarean delivery
in preventing neonatal HSV infections is unknown, and this practice has been recently challenged in two large studies in which infected
infants were born in the presence of intact membranes.3
17
Emendation 2006:
HERPES SIMPLEX VIRUS
Algorithm 1 and 2: HSV in pregnancy: risk assessment/management of
neonatal disease
Caesarean section reduces risk of HSV transmission in women shedding HSV
at the time of birth, particularly in women with first time infections who are
HSV type specific antibody negative. E9
H E R P E S
S I M P L E X
A L G O R I T H M
V I R U S
Herpes Simplex Virus Infections

in Pregnancy: Neonatal Management
Low risk
of neonatal HSV disease
ie mother with recurrent
infection, or primary infection
seroconverted well prior
to delivery
Collect surface swabs at 24

hours of life eye, throat,
umbilicus, rectum, urine
High risk of neonatal HSV disease

ie mother with primary infection
close to delivery or infant born
through birth canal with active
HSV disease to mother with no
prior history of genital HSV
Perform:
Follow for signs of infection
LFTs
HSV PCR on blood (if available)
Positive surface swab

or sick newborn
Commence IV aciclovir
immediately, duration
will depend on surface
culture & CSF results
surface swabs at birth

(onset of clinical signs) eye,
throat, umbilicus, rectum, urine
blood count (for low platelets),
Perform lumbar puncture

(CSF analysis, viral culture,
PCR for HSV DNA), blood count
(for low platelets), LFTs, & HSV
PCR on blood (if available)
Infant with
clinical signs of
neonatal HSV disease
(regardless of
maternal history)
Commence IV aciclovir
immediately from birth
If clinical signs of HSV disease
develop, perform LP (CSF
analysis, viral culture, HSC PCR),
CNS imaging and repeat blood
count, LFTs.
Vesicular skin lesions or

atypical pustular or
bullous lesions, especially
on presenting part
Seizures
Unexplained sepsis with
ve blood cultures not
responding to antibiotics
Low platelets
Elevated LFTs
DIC
Respiratory distress
(after day 1 of life)
Corneal ulcer/keratitis
ACICLOVIR THERAPY
Oral therapy should not be used for empiric or
therapeutic treatment of HSV in the neonate.
The current recommended dose is 20 mg/kg/dose IV,
3 times/day as 12 hour infusion. For disease confined to skin,
eye, mouth: duration of therapy is 14 days. For encephalitis,
disseminated disease: 21 days is recommended.7
Follow up:
NOTES
The incidence of neonatal HSV disease in Australia is approximately
3.0 per 100,000 live births.9
Survivors should be monitored closely for recurrences, eye disease,

CNS sequelae. LP should always be performed on all infants with
suspected HSV relapse to exclude CNS involvement.
A phase I/II trial of oral aciclovir to prevent adverse neurological outcome
in infants with frequent cutaneous recurrences after HSV-2 skin, eye,
mouth disease demonstrated neutropenia in 50%, development of
aciclovir-resistant virus in 4% and reduction of cutaneous recurrences
(CNS outcome was not studied).8 Until results of larger, ongoing phase III
trial available, suppressive therapy cannot be routinely recommended.
18
H U M A N
I M M U N O D E F I C I E N C Y
A L G O R I T H M
V I R U S
Diagnosis of HIV Infection

in Pregnant Women
Possible indications for testing
1. Recipient of blood product or human tissue pre1985
2. Past history of intravenous drug use (IDU)
3. Partner of person with IDU or resident/partner from high prevalence area
4. Bisexual relationship
5. Seroconversion illness
Routine antenatal
screening? 1(a)
PRE-TEST COUNSELLING
HIV ANTIBODY
Screen with ELISA
Confirm with Western blot (WB)
ve
+ve
POST-TEST COUNSELLING
Refer to physician specialising

in HIV infection or physician
with access to HIV expertise
Obstetric care in conjunction
with above
Paediatric HIV prenatal counselling
(SEE ALGORITHMS 24)
Lab testing(b)
Should include
HIV RNA
viral load
Repeat in 4 weeks if recent exposure

or indeterminate Western blot
+ve
No further follow up with

respect to HIV unless
re-exposure occurs or risk
behaviour continues
ve
Antiretroviral (ARV) therapy3

see General Principles of ARV in Pregnancy,
ALGORITHM 3
Routine
antenatal
ultrasound
As per routine
obstetric care
unless complications
anticipated
CD4 +ve
lymphocyte subsets
Others:
e.g. FBE, LFT, U&E/Creat
NOTES
a. As effective strategies to prevent perinatal HIV transmission exist, knowing the HIV status in pregnant women may be warranted. Half of HIV +ve pregnant women are unaware of their HIV status
and two-thirds have no risk factors.2
b. Consideration should be given to resistance testing and/or viral subtyping if HIV acquired outside of
Australia.
19
Serology for:
Syphilis
Hep B & C
CMV, HSV
Toxoplasma
Chlamydia screen
H U M A N
A L G O R I T H M
V I R U S
Assessment of Risk Factors in

Perinatal Transmission of HIV
Fetal Risk Assessment & Counselling
Based on figures before the use of routine Highly Active Antiretroviral Therapy (HAART) in management of HIV in adults.
Viral Load
(VL)(HIV RNA
level)
Undetectable
(UD) ie < 400
copies HIV
RNA per mL
by non-ultra
sensitive
assays
Graded levels of
risk, with UD to
1000 copies/mL
carrying the
lowest risk and
> 100,000
copies/mL the
highest risk.
NB: no "safe"
viral load
identified4,5
CD4+
lymphocyte
count
Detectable
Gestation
<37 w
Rupture Of
Membrane (ROM)
> 4 hours
Mode
of delivery
37 w
Breast
Vaginal
(VD)
Approximate
linear inverse
relationship
between CD4
count and risk6
4-fold
in risk7
Approximate
linear inverse
relationship
between
gestational
age and risk6
Mode
of feeding
Caesarean
Doubling of
risk with VD8
Doubling of
risk with breastfeeding9,10
COMMENTS
Other relative risk factors include the first born twin and the presence of co-infections (eg sexually transmitted diseases and
chorioamnionitis).
Antenatal tests as per routine obstetric follow-up. Also, see ALGORITHM 1.
Apart from risk assessment, counselling should include
strategies to prevent transmission (see ALGORITHM 3)
management of baby at birth, including ARV and prophylaxis
testing of baby
care plan before delivery
care plan for future with respect to a family that has HIV "infected" and HIV "affected" members.
20
Bottle
H U M A N
A L G O R I T H M
V I R U S
Strategies to Minimise
the Perinatal Transmission (PNT) of HIV
HIV +ve pregnant women
See General Principles of
ARV in Pregnancy
On antiretroviral therapy (ARV)

(either treatment or prophylaxis)
NO
YES
Presents in labour
Mode of
delivery (a)
Obstetric
care and delivery11
NO
(c)
YES
Formula
feed
IV AZT
Vaginal
VS
+/-
NEVIRAPINE
(NVP)12 (d)
Elective
Caesarean section(b)
IV AZT 3 hours before section
(see Appendix 1)
Caesarean section
Consider if VL >1000
copies/mL or unknown or if
ROM <4 hours (e)
ALGORITHM 4
Follow up with 6
weeks AZT to
infant +/ one
dose NVP if
indicated
ALGORITHM 4
Formula feed
COMMENTS
See Table 1 for estimated PNT risks by selected strategic options.
a If a pregnant woman is already on HAART, the added benefit of caesarean section may be marginal particularly if viral load is undetectable. The combined risk estimates for vertical transmission for women already on an AZT containing regimen is 1 12% (mean
5.7%) with HIV RNA level near delivery of 1000 10, 000 copies/ml and 9 29% (mean 12.6%) if HIV RNA levels are > 10, 000
copies/ml. Based on this, the American College of Obstetricians recommend elective caesarean section as an added strategy if VL >
1000 copies/ml. http://hivatis.org/guidelines
b If labour commences before planned caesarean section and membranes are ruptured for < 4hours, semi-urgent elective caesarean section should be considered (especially if not on ARV prophylaxis and viral load detectable). (see comment e)
c Includes avoidance of invasive procedures e.g. fetal scalp electrodes, episiotomy. If resuscitation needed, gentle oral suction of baby
only (if possible). Wash baby down as soon as possible after birth.
d HIVNET 012: Single dose NVP, 200 mg, to mother intrapartum, and follow up with single dose to infant (2mg/kg) within 3 days of birth.
Caution: Preliminary data report NVP resistance in some mothers and infected infants after a single dose in HIV NET 012 study.
Significance not currently known.14 The role of additional NVP prophylaxis when a woman is already on an established ARV regimen is
unknown and currently not recommended.15
e The value of caesarean section in reducing HIV PNT after a short duration of ROM has not been established. However as a continuum
of PNT risk following ROM exists, some would perform caesarean section to shorten labour and hence duration of ROM.
21
H U M A N
A L G O R I T H M
V I R U S
Management of Infant
at Risk of Perinatal HIV
At Birth Clinical Assessment
a,b
Commence antiretroviral (ARV) prophylaxisc
LABORATORY FOLLOW-UP
See Table 2
PCR
(DNA)
Virus
isolation
CLINICAL
HIV
antibody
Review at times of testing

Clinical examination +
neurodevelopmental assessment
Routine childhood vaccination
except inactivated polio (s/c)
instead of oral polio vaccine
(rationale: HIV infected
household member(s) at risk of
polio from polio faecal excretion
in vaccinee)
Seroreverters: Follow till
adulthood to monitor continued
health after in-utero exposure to
ARV
MEDICATIONS
ARV to stop at 6 weeks

Start co-trimoxazole
(0.5 mLs/kg, daily)
Stop co-trimoxazole when
testing at 3 months confirms
absence of HIV infection in a
non-breast fed infant
COMMENTS
a No HIV embroyapathy syndrome has been described.
b A third of perinatal HIV transmission occurs in utero and 2/3 during the peripartum period. Hence, infected infants are less likely to present
with signs and symptoms of HIV at birth. Definitions: "in utero transmission" = +ve PCR result < 7 days of age. "peripartum transmission"
= +ve PCR result 7 days of age.
c Postnatal ARV Regimen: AZT is recommended, regardless of the mothers therapy. Zidovudine (AZT syrup,10 mg/mL), 4mg/kg/dose B.D.
to start within 8 hours of delivery, given for 6 weeks. The benefit of adding 3TC to AZT postpartum for 6 weeks if mothers have been on
combination of antiretrovirals during pregnancy is unclear. If added, dose of 3TC solution (strength, 10 mg/mL) is 2 mg/kg/dose B.D. to
start within 8 hours of delivery, for 6 weeks. If nevirapine is indicated, 2 mg/kg, single dose, to be given within 3 days of birth. No
confirmed short/medium term adverse events associated with in-utero/postnatal exposure to AZT. Concern with mitochodrial toxicity after
AZT +/- 3TC exposure in-utero remains to be confirmed.
d Any positive virological test (PCR or virus culture) must be confirmed on a separate sample due to the potential for false +ve results.
PCR has equivalent sensitivity of detection as virus isolation but is available sooner (takes ~1 week) than viral culture (46 weeks).
Close to 100% sensitivity of detection at 3 months in non-breast fed infants.
Traditionally, seroreversion i.e. disappearance of passive (maternal) antibodies is documented before declaring a child uninfected.
Antibody testing after 6 months may be useful to document declining maternal antibodies titres in uninfected babies.16
22
H U M A N
T A B L E
V I R U S
Perinatal Transmission (PNT) Risk Estimates

by Selected Intervention Strategies
ANTIRETROVIRALS
Mother
Pregnancy
Mother
Intrapartum
Baby
Delivery
Feeding
Vaginal
Formula
20%
Vaginal
Breast
40%
Vaginal
Breast
~36%
Caesarean
Formula
10%
(Full course AZT, 076 Study)
Vaginal
Formula
8%
19998
Caesarean
Formula
2%
Baseline(a)
Dunn, 19929
Nduati,
200010
(Uganda)(b)
The International Perinatal HIV Group,

199413
Connor,
The International Perinatal HIV Group,

Shaffer,
199917
19998
Vaginal
Formula
10%
Wade,
199818
Vaginal
Formula
10%
Wade,
199818
Vaginal
Formula
20%
NVP
NVP
Vaginal
Formula
~10%
Guay,
199912
(Short course AZT, Thai study)
PNT Risk
(HIV NET 012, Uganda)
Key: Shaded rows represent risks when no intervention strategies are in place. 0 = no ARV prophylaxis, + = ARV given. Unless stated, the
antiretroviral referred to is AZT. NVP = nevirapine
a
Prior to the introduction of recommended intervention strategies, a child born to an "asymptomatic" HIV infected woman with CD4+
counts > 200c/mm3 who did not breast feed had ~20% of being infected perinatally (in developed countries). For the purpose of these
algorithms, this figure is referred to as the "baseline" and increases or decreases in risk are referable to this baseline.
b
The approximate doubling of risk in breast fed babies over formula fed babies in this randomised clinical trial was seen over a range of
breast feeding duration (6 weeks to 2 years), with 75% infected in the first 6 months of breastfeeding.
T A B L E
GENERAL PRINCIPLES OF ARV IN PREGNANCY

1. ARV regimens are either treatment schedules or regimens
for preventing perinatal transmission (prophylaxis).
Women are now generally on HAART at time of pregnancy.
2. Pregnancy should not preclude use of optimal therapeutic
regimen.3 If initiating therapy, consideration could be given
to waiting till the second trimester. A possible association of
pre-term delivery with combination therapy has been found
but not confirmed. http://hivatis.org/guidelines
3. Efavirenz and hydroxurea (teratogenesis, animal studies)
are not recommended in pregnancy. Caution has been
raised with d4T + ddI in combinations with protease
inhibitors in pregnancy (fatal lactic acidosis. Pharmaceutical
company drug alert, January 2001)
4. The three part ZDV prophylactic regimen (Protocol 076) is
considered best practice, and is recommended for all pregnant women with HIV infection regardless of RNA viral
load.13 (Appendix 1) Thus, ZDV should be included as a
component of antenatal regimen where possible. If ZDV is
not included antenatally, intrapartum and newborn ZDV are
still recommended. However, if d4T is part of antenatal
ARV regimen, intrapartum ZDV is not recommended
because of potential drug interaction.
Suggested Testing Regimen

TESTS
Time
T Cell
Subsets
(Day 1)
PCR
Virus
HIV
Isolation Antibody
(+)
Week 1
Week 6
3 months
(+)
6 months
(+)
(+)
12 months
18 months
(if still seropositve at 12 mo)
Texts in parenthesis denote optional time or type of test.
APPENDIX 1: PACTG 076 ZIDOVUDINE REGIMEN13

Regimen
Time of ZDV
Administration
Antepartum
Intrapartum
Postpartum
Oral administration of 100 mg ZDV 5 times daily*, initiated at 14-34 weeks gestation and continued throughout the pregnancy.
During labour, intravenous administration of ZDV in a one-hour initial dose of 2 mg/kg body weight, followed by a continuous infusion of 1 mg/kg body weight/hour until delivery.
Oral administration of ZDV to the newborn (ZDV syrup at 2 mg/kg body weight per dose every six hours) for the first six
weeks of life, beginning at 8 -12 hours after birth.** (Note: intravenous dosage for infants who cannot tolerate oral intake
is 1.5 mg/kg body weight intravenously every six hours).
* Oral ZDV administered as 200 mg three times daily is an acceptable alternative regimen
** 4 mg/kg per dose, twice daily is an acceptable alternative regimen
23
Emendation 2006:
HUMAN IMMUNODEFICIENCY VIRUS
Nevirapine toxicity in women: The risk of hepatic toxicity is increased in
women particularly if CD4 counts are > 250 c/ml, usually in the first 6 weeks
of starting therapy. Pregnancy may be an added risk factor. Thus, caution is
warranted and close monitoring recommended if this agent is included in
therapeutic/prophylactic HAART regimens started during the antenatal period.
E10
Erratum, Table 1: In the Guay 1999 study (HIV NET 012), infants were breast
fed (not formula fed)
Revised suggested postnatal testing times and review

*HIV PCR at 1, 6, 12 weeks and at 6 months. Virus isolation and Tcell subsets are no longer routinely done in this setting.
If all PCRs remain negative, then clinical review only is recommended
at 12 months. HIV antibody at 18 months to document sero-reversion
builds further confidence in the diagnosis of non-infection in the
infant.
Nb: * As the proviral DNA PCR is currently not commercially available (2006), HIV
RNA PCR is used.
L I S T E R I A
A L G O R I T H M S
&
Diagnosis of Suspected Listeriosis and

Management of Proven Maternal Infection
Unwell febrile pregnant women
(includes flu-like illness)
Blood cultures
Gram stain and cultures
of genital tract
amniocentesis
Gram stain and culture
Positive for
Listeria monocytogenes
Negative
Consider other infections

and empiric antibiotics
Serious infection
including amnionitis
Mild
infections
Amoxycillin/Ampicillin
(46 g/day IV) and
Gentamicin for 14 days1, 2
Amoxycillin/Ampicillin
(23 g/day po)
for 14 days1, 2
Urgent delivery depending

on severity of maternal illness
and gestation
NOTES
Maternal listeriosis in 2nd/3rd trimester results in a mortality of 4050% for the fetus
Serology is not a useful tool for diagnosing listeria3
Early treatment of maternal infection can improve perinatal outcome
The recommended treatment regimens above are based on observations and case
reports. No randomized controlled trials have been performed to establish optimal
treatment regimens or to support efficacy of penicillin over ampicillin, but ampicillin or
amoxycillin is generally considered the preferred agent.13
Synergism exists for penicillin or ampicillin with gentamicin.3
Trimethoprim/sulphamethoxazole is suggested as an alternative in the penicillin allergic
patient.
24
L I S T E R I A
A L G O R I T H M
Antenatal Prevention Strategies

for Perinatal Transmission of Listeria
Pregnant women
Avoid
High Risk Foods
Use Safe
Food Handling Practices
Unpasteurized milk or food made

from raw milk
Thoroughly cook raw food from

animal sources
Pate, dips and soft cheeses
Chilled precooked seafoods
Keep uncooked meat separate

from vegetables, cooked foods
and ready-to-eat foods
Precooked meats and meat

products which are eaten without
further cooking or heating
Eat freshly cooked foods.

Avoid eating dips and salads in
which raw vegetables may have
previously been dipped
Thoroughly wash raw fruit

and vegetables
Reheat left-over or ready-to-eat

food until steaming hot
Uncooked or smoked seafood
Pre-prepared salads and coleslaws
Past history of listeriosis:

No role for vaginal cultures
NOTES
* Intrapartum antibiotic therapy is not recommended for mothers with a past history of perinatal
listeriosis. No data to suggest reculture during subsequent pregnancy has any value
* Asymptomatic vaginal carriage of L. monocytogenes is rare. Faecal carriage of L.
monocytogenes is found in 0.616% of the population at any one time.4 The significance of
faecal excretion in perinatal infection is uncertain.
* If listeria found on vaginal/rectal culture, it may be appropriate to try to eradicate the
organism before delivery with oral amoxycillin or erythromycin (250 mg q6hrly for 10 days).
While this approach may seem reasonable it has not been definitively studied.5
* Local Public Health Department publications, with detailed advice, are available.
25
L I S T E R I A
A L G O R I T H M
Diagnosis and Management of

Infant at Risk of Perinatal Listeriosis
Maternal listeriosis
(proven or suspected)
Still
birth
Unwell neonate
Suspicious clinical findings:
placental, cord or postpharyngeal granulomas
Multiple small skin
granuloma, papular or
pustular skin rash
Meconium stained liquor
<34 weeks gestation
Purulent conjunctivitis
Well
neonate
NOTES
Mortality rates from 350% in
infected neonates born alive7
Perinatal listeria can present as

early-onset disease (within 7 days
of birth) often associated with
prematurity and fulminant disease,
and late onset disease (7 days to
6 weeks), often presenting with
meningitis.
Surface cultures with Gram stain
from placenta, meconium, rectal
and external ear canal have all
been found to have a high yield in
isolating the organism.5, 8
Optimal antimicrobial therapy for
various manifestations of listeriosis
has not been established in
controlled clinical trials and
remains controversial. No
controlled trials available to
establish a drug of choice or
duration of therapy.13
Alternative antibiotics:
Trimethoprim/sulphamethoxazole
reserved in the of event of lack of
response to standard therapy;
Rifampicin effective in vitro but
inadequate clinical information
available; erythromycin sensitive
but bacteriostatic; no role for
cephalosporins.
Septic workup
Blood cultures, CSF
Superficial cultures
with Gram stain
Culture placenta
CXR, Urine culture
FBC
Empiric treatment:
Amoxycillin/ Ampicillin (50 mg/kg q12hrly)
and gentamicin (2.5 mg/kg q12hrly)6,7
Culture positive or unwell at

diagnosis: continue antibiotics
CSF positive:
Amoxycillin/Ampicillin and
gentamicin 21 days
CSF negative:
Amoxycillin/Ampicillin and
gentamicin 14 days
26
Well neonate and

culture negative:
Stop antibiotics at
48 hours
M Y C O B A C T E R I U M
T U B E R C U L O S I S
A L G O R I T H M
Antenatal Diagnosis
Symptoms
suggestive
of TB
HIV
positive
Close contact of
infectious TB
Recent arrival from area

with high prevalence of TB
Mantoux test
Negative
Positive
No further action
High clinical suspicion
Examine for signs of TB +

Perform chest X-ray*
No evidence
of TB
Evidence of old
pulmonary TB
Evidence of
active TB
Mantoux conversion
> 2 years or unknown
High risk** or Mantoux

conversion within previous
2 years
Sputum, urine +/- other

specimens, or investigations
as appropriate
Reassess need for INH

prophylaxis post partum
INH prophylaxis from

2nd trimester
ALGORITHM 2
* Chest X-ray may be omitted if the risk of active TB is considered to be low.

** High risk HIV positive, those with medical conditions that increase the risk for reactivation of inactive TB, eg diabetes, chronic renal
failure, malignancy.
NOTES
The development, clinical presentation and progression of TB
are not altered by pregnancy.1,2
Although data are conflicting, pregnancy is not thought to
increase the risk of inactive TB becoming active.
The symptoms of extrapulmonary TB are frequently non-specific,
and may be attributed to physiological changes of pregnancy.
Areas with high prevalence of TB include South East Asia,
Pacific Islands, Africa, Eastern Europe, Latin America.
Mantoux testing of contacts is usually performed by local Health
authorities, and may need to be repeated at 12 weeks after
break of contact.
Mantoux skin testing: intradermal injection of 0.1 mL of a 100
international unit/mL solution of purified protein derivative (PPD),
with induration measured at 48-72 hours.
The Mantoux test is not affected by pregnancy.
Chest X-ray should be performed with appropriate abdominal
shielding.
Isoniazid (INH) "prophylaxis" is not true prophylaxis, and is often

referred to as "treatment of latent TB infection". Usual duration is
6 months.
INH is safe in pregnancy.3
Pyridoxine should be given with INH to pregnant and breastfeeding women (50 mg/day), and to their breast-fed infants (10
mg/day) whether or not the infant is taking INH.4,5
Interpretation of Mantoux skin test positivity [Source: American
Thoracic Society, 1999]
5 mm diameter in people with HIV infection, in people in close
contact with someone with infectious TB, or in people with a
chest X-ray suggestive of previous TB;
10 mm diameter in recent arrivals (< 5 years) from high prevalence areas, in injecting drug users, residents/employees of prisons, homeless shelters, residential facilities for AIDS patients,
high risk patients** or in children < 4 years old;
15 mm diameter in those 4 years old with no risk factors for
TB, and in children who have had BCG.
27
A L G O R I T H M
Initial Management of
Suspected Maternal TB
Proven maternal TB
Low risk of
INH resistance
INH
Rifampicin
Ethambutol
Use of Pyrazinamide is optional*
High risk of
INH resistance
INH
Rifampicin
Ethambutol
Pyrazinamide
9 months
9 months
2 months
6
6
2
2
months
months
months
months
NOTES
Active TB during pregnancy must be treated immediately. This is true for cases in which TB has not been confirmed,
but is considered likely on clinical grounds.
TB does not affect the course of pregnancy or type of delivery required.1,2
High risk of INH resistance should generally be assumed, particularly for HIV-positive women, recent arrivals from an area of high
prevalence, and those who have had previous anti-TB treatment.
Duration of therapy with each drug may vary according to the resistance pattern of the isolate, and according to the form of TB
(e.g. longer for TB meningitis).
*The duration of treatment with INH and Rifampicin is longer for cases when Pyrazinamide is not given in the first 2 months.
Directly observed therapy (DOT) is ideal practice, but may not be feasible for all patients with TB (the states vary on the application of
DOT).
All of the anti-TB drugs cross the placenta and reach a low concentration in fetal tissues.3 However, INH, Rifampicin and Ethambutol
are all safe in pregnancy. Little is known about the effects of Pyrazinamide in pregnancy, but it has been used without adverse
effects. Many internationally recognised TB organisations recommend its routine use in pregnancy.6 Streptomycin is contraindicated
in pregnancy.6
The risk of INH-induced hepatotoxicity appears to be higher in women, and may be more so in the perinatal period. Women should
be monitored for hepatotoxicity with monthly ALT/AST.7
300 mg po daily (give with Pyridoxine 50 mg daily note increased dose in pregnant and
INH
breastfeeding women).
450 mg po daily (< 50 kg)

Rifampicin
600 mg po daily ( 50 kg).
15 mg/kg po daily.
Ethambutol
Pyrazinamide
1.5 g po daily (< 50 kg)

2 g po daily ( 50 kg).
28
A L G O R I T H M
Management of the Neonate

Maternal TB is likely
to be associated with
haematogenous spread*
Active pulmonary TB
mother infectious
at time of delivery
Assess neonate
for clinical evidence
of congenital TB
Mother on
anti-TB treatment
not infectious
Mother completed
anti-TB treatment
not infectious
Assess neonate
of congenital TB
Assess neonate
of congenital TB
Absent
Present
Absent
Chest X-ray and

gastric aspirates x 3
Chest X-ray, gastric aspirates

x 3 and lumbar puncture
INH for
6 months
Mantoux test
at 3 months
and 6 months
No evidence
of TB
TB
INH, Rifampicin, Pyrazinamide

+ Amikacin or Ethionamide
INH for
6 months
Positive at
any time
Investigate according to clinical

state and treat as above
Positive at
any time
Mantoux test
at 3 months
and 6 months
Negative at
6 months
BCG should be given if there is

any possibility of future
exposure to TB
Negative at
6 months
Absent
Mantoux test
at 3 months
* Disseminated or miliary TB, tuberculous meningitis, etc. The placenta or maternal genital tract may become infected, and congenital
infection may ensue. However, congenital TB remains very rare.7,8
Sputum smear positive
NOTES
Most cases of neonatal TB occur as a result
of airborne spread after delivery. However,
separation of mother and neonate is only
necessary if the mother is sick enough to
require hospitalisation for TB.5
Other family members and close contacts
should be assessed for TB infection or
disease. If a close contact is infectious,
separation is preferable, but, if impossible,
INH prophylaxis should be given until the
contact has been culture-negative for 3
months.
Respiratory distress,hepatosplenomegaly,
fever, lymphadenopathy and poor feeding
are the most common presenting features
of congenital TB.8,9
If congenital infection is suspected, the
placenta should be examined and
microscopy, culture and histology performed.
susceptibility results are available.

The Mantoux test is likely to be negative for
the first few weeks of life, even if the
Ethionamide or Prothionamide 1520
neonate has TB.3,4,10
mg/kg daily until drug susceptibility results
are available. May be difficult to obtain.
Mantoux conversion may be delayed for up
to 6 months; thus INH prophylaxis must be Ethambutol 15 mg/kg po daily may be used
continued until this time.
in place of Amikacin or Ethionamide, but
should be reserved for special cases. It
Drug treatment
may induce optic neuritis, which is difficult
The decision regarding number and choice
to identify in infants.
of drugs for management of neonates and
Streptomycin 1520 mg/kg im daily may
infants with TB is difficult, and warrants
also be used in place of Amikacin or
specialist advice.
Ethionamide, but injection is painful and it
INH 5-15 mg/kg po daily for 6 months
is difficult to obtain.
(Pyridoxine 10 mg po daily must be added
These drugs are excreted in breast milk.
for breastfed infants).
If a breastfeeding mother and neonate are
Rifampicin 1020 mg/kg po daily for 6
both on anti-TB therapy, there is a small
months.
risk of toxic levels in the neonate. This can
Pyrazinamide 1530 mg/kg po daily until
be minimised if the mother takes her
drug susceptibility results are available.
medications immediately after a breast
Amikacin 15 mg/kg iv daily until drug
feed.
29
P A R V O V I R U S
A L G O R I T H M
Parvovirus B19 Infections During

Pregnancy: Risk Assessment
EXPOSURE DURING EPIDEMIC
Risk of infection if susceptible

after exposure at home
is up to 50%1
60% of women of childbearing age are immune

to parvovirus infection1,3

after exposure at school or
child care = 2030%1,2

after exposure in community
is up to 20%
40% of women of child-bearing age are

susceptible to parvovirus infection3
RISK OF INFECTION IN PREGNANCY
50% x 40%
20%
2030% x 40%
= 812%
20% x 40%
8%
3% hydrops (between 9
and 20 weeks gestation)4,5
<1% (no excess)

congenital abnormalities4,5
OUTCOME
(PROVEN MATERNAL
INFECTION)5,6,7
10% excess fetal loss in
first 20 weeks of pregnancy4
32% spontaneous
resolution (usually
within 8 weeks)
NOTES
It is not practicable to prevent
exposure at home. Exclusion from
work of pregnant school teachers
or child care workers is not
recommended during a parvovirus
epidemic (nor is exclusion of
infected children).
Susceptible pregnant HCW should
not care for patients with known
complicated parvovirus infection (eg
aplastic crisis) or chronic parvovirus
infection (eg in an
immunocompromised host).
Routine antenatal screening is not
33% death without IUT

(usually within 45 days of
first abnormal ultrasound)
indicated.
There is a 50% risk of transmission
from an infected mother to her
fetus.8
Fetal loss = 15%, compared with
5% overall (ie excess loss = 10%).4
Onset of hydrops 2-17 weeks
(average 5 weeks) after maternal
infection.
Congenital abnormalities
anecdotal reports only (less than
rate of major malformations in
newborns of 2%).4,5
IUT = intrauterine transfusion.
30
27%
resolution
after IUT
6%
death after
IUT
OVERALL RISKS
Pregnant woman with
Any pregnant woman
exposed to parovovirus proven recent infection
Excess fetal
loss in first
20 weeks
Death from
hydrops
or its
treatment
0.41%
(1 in 1001 in 250)
5%
(1 in 20)
0.050.1%
(1 in 8501 in 2000)
0.6%
(1 in 170)
Pregnant women who are exposed should be informed

of risks, and offered serological testing.
P A R V O V I R U S
A L G O R I T H M
Parvovirus B19 Infections During Pregnancy:

Antenatal Diagnosis and Management
DIAGNOSIS OF INFECTION FOLLOWING CONTACT OR ILLNESS
WITH RASH DURING PREGNANCY9,10
(Check rubella serology symptoms are similar and cross-reactions can occur)
SEROLOGY
INTERPRETATION
ACTION
IgG +
IgM
IgG
IgM
IgG
IgM +
IgG +
IgM +
Immune
Susceptible
? Recent
infection*
Recent
infection
Nil
Repeat IgG 24 weeks after exposure

or if symptoms occur
IgG
(false positive IgM)
IgG +
(recent infection)
See
ALGORITHM 3
NOTES
IgM is detectable within 13 weeks of exposure and usually remains
detectable for 23 months.
IgM reference standard: mu-capture radioimmunoassay (MACRIA).
Commercial IgM test kits (EIA or IF):
sensitivity: 70-80% overall (100% in adults with arthropathy; lower in children)
specificity: 92-97% overall (70-85% in patients with other infections, including rubella)9
Note: absence of IgM does not exclude recent infection
* Symptoms include non-specific illness, rash, and/or arthralgia/arthritis).
31
P A R V O V I R U S
A L G O R I T H M
Parvovirus B19 Infections During Pregnancy:

Management of Proven Maternal Infection
RECENT MATERNAL INFECTION
Ultrasound examinations at
12 week intervals for 612 weeks
after maternal infection5
Normal
Fetal hydrops
No
further action
Refer to specialist experienced

in fetal ultrasound, blood
sampling and transfusion
Fetal blood
sampling
Daily
ultrasound
Resolution
Mild anaemia, normal

platelets, reticulocytosis
Moderate to severe anaemia

+/- thrombocytopenia
IUT
Fetal blood
sampling
Progression
NOTES
No intervention is available to prevent fetal infection or damage.
Termination is not indicated because of low risk of fetal damage.
Amniocentesis for diagnosis of asymptomatic intrauterine fetal
infection is not recommended.
a-fetoprotein levels are not helpful previous reports that
increased levels predict poor outcome have not been confirmed.5
Pregnancy should be monitored by repeated ultrasound
examination to detect hydrops fetalis.

A fetus with mild hydrops may be profoundly anaemic.
Fetal blood sampling measure haemoglobin, platelets and
reticulocyte count.
No specific investigation is indicated in normal infants.
Infants in whom hydrops has occurred and resolved should be
monitored for evidence of anaemia.
32
R U B E L L A
A L G O R I T H M
Diagnosis of Suspected
Maternal Rubella Infection
Indications for testing pregnant women
a) Routine antenatal screening (IgG only)*,1,2

If IgG ve, immunize after delivery
If IgG +ve; if >10 IU/mL; minimal risk of reinfection
If <15 IU/mL; consider reimmunisation after delivery
b) Rubella testing (IgG/IgM)** because of

(i) contact with rubella
(ii) rubella-like illness (fever, erythema, arthralgia)
IgG +ve
IgM +ve
Possible recent infection
(or reinfection,
depending on history)
Repeat to
confirm
IgG ve
IgM ve
Susceptible
IgG ve
IgM +ve
Possible recent infection
Repeat if <3 weeks

since contact or <7days
since onset of illness
Repeat
IgG seroconversion***
No seroconversion
Retest by EIA or HAI

on IgM fractions
after sucrose density
gradient centrifugation
Susceptible
(possible false
positive IgM)
Positive
IgM
confirmed
Counsel and manage as per ALGORITHM 2
Immunise after delivery
33
IgG +ve
IgM ve
Past infection
or immunisation;
manage as for positive
antenatal screening
NOTES
*Different laboratories
use various cut-offs for
reporting low IgG levels
ranging from 7 to as high
as 50 IU/mL. Levels
corresponding to
protection from
reinfection are
imprecise, but only a
small proportion of
women are affected by
reinfection.1,2
** Reinfection can occur
without detectable IgM.
Previously stored serum,
if available, should be
retrieved and tested in
parallel with current
serum, for evidence of
pre-existing antibodies
or seroconversion.
*** Seroconversion
should be checked by
testing the sera in
parallel.
R U B E L L A
A L G O R I T H M
Management of Proven
Maternal Rubella Infection
Maternal infection*
Primary infection
Reinfection
Risk of fetal damage or

congenital rubella syndrome (CRS)
related to timing of maternal infection59**
< 8 weeks
90100%
812 weeks
50%
If asymptomatic reinfection with a reliable

history of previous positive serology, then
risk of fetal damage is <5%3,4
If typical clinical rubella or doubtful
previous immunity, risk must be assumed
to be the same as for the first infection
1220 weeks
20%
>20 weeks
< 1%
Consider termination of pregnancy if maternal infection in first trimester.

If maternal infection occurred in second trimester, consider fetal testing.
Prenatal fetal diagnosis/testing

Rubella PCR, rubella culture and fetal IgM can be performed following
chorionic villus sampling (CVS)/amniocentesis or cordocentesis9,10 ***
BUT
CVS is associated with risk of contamination with maternal tissue
giving false +ve PCR
PCR is not widely available and sensitivity is generally not well
validated. However, a positive result will be helpful
(assuming that contamination can be excluded)11
False negative fetal IgM is common until late in pregnancy 10,12
NOTES
* No specific management of mother (rubella specific immunoglobulin not available and normal human immunoglobulin NOT indicated).
** Transmission risks and details of incidence and type abnormalities can be found in textbooks8,9
*** Contact your local Public Health Virology Laboratory for information about the availability of rubella culture or PCR
34
R U B E L L A
A L G O R I T H M
Management and Follow Up

of the Infant at Risk of Infection
At birth
Ensure clinical attendants are rubella vaccinated and have specific
antibodies detected
Examine infant for evidence of CRS (growth retardation, eye/cardiac
abnormalities, rash, haematological abnormalities, pneumonitis,
osteitis are most likely to be detectable at birth)
Investigate infant
Serology (IgM)
PCR (urine and throat swab); note -ve PCR does not exclude infection
Culture urine and throat swabs, tears (conjunctival swab),
lens tissue (if available); results can take several weeks
Clinical features CRS

IgG maternal IgG titre
(measured in parallel)
IgM +ve
PCR +ve
No clinical features CRS

IgM +ve
PCR +ve
No clinical features CRS

IgG maternal IgG titre
(measured in parallel)
IgM ve
PCR ve
Symptomatic, infected infant
Asymptomatic, infected infant

(risk of late onset disease
months or years after birth)
Infant probably not infected
No specific management
Breastfeeding not contraindicated
Ensure ophthalmology, cardiac and hearing assessments at birth
Regular assessments (3 to 6 monthly) necessary in the first few

months and years of life to detect the emergence of
abnormalities related to persisting infection (deafness,
neurological deficiencies, epilepsy, cataracts, retinopathy, tooth
defects and growth retardation)13
Infants infectious for at least 12 months after birth and are a
hazard to susceptible female staff and pregnant contacts
Infant should be isolated (droplet and contact) while in hospital
Ensure all hospital contacts/caregivers are rubella immune
35
Reassure
Breastfeeding not
contraindicated
Confirm absence of infection
with falling/absent IgG at or
after 9 months of age
S T R E P T O C O C C U S ,
A L G O R I T H M
G R O U P
Management of Pregnancy with Respect

to Group B Streptococcal (GBS) Infection
Strategy A*
Prenatal screen for maternal GBS
colonisation
Strategy B
Obstetric
Risk factors alone
Screen at 3537 weeks gestation

Low vaginal + anorectal swabs **
Selective broth medium
GBS
colonisation
GBS
negative
GBS unknown (failed

screening, refused swab or
result unavailable)
Obstetric risk
factor(s)***
No chemoprophylaxis
unless previous infant
with GBS infection or
GBS bacteruria
(current pregnancy) of
any colony count.
Yes
Intrapartum chemoprophylaxis
(SEE ALGORITHM 2)
Obstetric risk factors ***

Previous infant with EOGBS
GBS bacteriuria (any colony count) this
pregnancy
Spontaneous onset of labour
< 37 weeks gestation
Rupture of membranes 18 hrs
Intrapartum fever 38oC
Nil
One or more
present
No
No chemoprophylaxis
Intrapartum chemoprophylaxis
(SEE ALGORITHM 2)
** Detection of GBS is increased by up to 25% by collecting an

anorectal swab in addition to a vaginal swab.6 A single swab may
be used, provided the vagina is swabbed prior to the anorectal
area. Samples may be obtained by the patient.
Maternal carriage of GBS does not predict premature rupture of
membranes or preterm delivery.7
Selective broth media are more sensitive than standard solid
media. Examples include NPC broth (Todd-Hewitt broth
supplemented with colistin, nalidixic acid and crystal violet) and
semi-solid new Granada medium.8
*** The obstetric factors listed are associated with increased risk
for EOGBS.2,9 However, 25-30% of cases are not associated
with maternal risk factors.2
Babies born to women with GBS bacteriuria (any colony count)
during pregnancy are more frequently and more heavily
colonised with GBS, increasing the risk of EOGBS.
NOTES
Colonisation of the genital tract with GBS occurs in
approximately 20% of women. Early onset GBS disease
(EOGBS, within the first week of life) occurs at a rate of 12 per
1000 live births, although this is declining.1
Intrapartum chemoprophylaxis is highly effective in reducing
neonatal colonisation with GBS and preventing EOGBS.1,2,3
* A recent Centers for Disease Control & Prevention (CDC) study
in >600,000 live births found the Screening approach >50%
more effective than the Risk Factor approach in preventing
GBS disease.4 The application of this in Australia remains to be
determined.
Prenatal screening (<35w) to detect GBS does not reliably
predict carriage at delivery. The later in pregnancy that cultures
are performed, the better the correlation with culture results at
delivery (particularly within 5 weeks of delivery).1,5,6
36
A L G O R I T H M
G R O U P
Intrapartum Antibiotic Prophylaxis for

Prevention of Early Onset Neonatal GBS Sepsis
GBS +ve, GBS -ve but previous infant with GBS
sepsis, GBS bacteruria (this pregnancy) or GBS
unknown with obstetric risk factors
GBS -ve or GBS unknown with no obstectric risk

factors
Signs of
maternal
sepsis
Signs of
maternal
sepsis
No
Give intrapartum chemoprophylaxis

Benzyl penicillin 1.2 g IV loading dose,
followed by 0.6 g IV 46 hourly, from
onset of labour until delivery
If penicillin hypersensitivity:
clindamycin 600 mg IV 8 hourly
OR
erythromycin 500 mg IV 6 hourly
Yes
Yes
No
Collect
Endocervical swab
Urine (m/c/s)
Blood cultures
Full blood count
CRP
Give broader spectrum antibiotics

amoxycillin 2 gm IV 6 hourly
+
gentamicin 46 mg/kg IV daily
+
metronidazole 500 mg IV 12 hourly
No antibiotics
NOTES
90% of neonates with EOGBS have onset of signs within 12 hours of birth (suggesting intrauterine transmission), so intrapartum antibiotic
prophylaxis is the most effective means of prevention.
The rate of fatal maternal anaphylaxis to penicillin is estimated at 1 in 100 000. Less severe reactions occur in 710%.
Clindamycin and erythromycin are active in vitro against GBS, but their efficacy in prevention of EOGBS has not been evaluated.
Clindamycin resistance has been reported in 3.4% of invasive GBS isolates, and erythromycin resistance in 7.4% (USA). Nonetheless,
they are recommended by most experts as alternatives for women who have hypersensitivity to penicillin.6
Pathogens responsible for chorioamnionitis include GBS, anaerobic cocci, and enteric Gram-negative bacilli (often polymicrobial).
37
A L G O R I T H M
G R O U P
Management of Infant Born to Mother

Who Received Intrapartum Prophylaxis
Signs of sepsis
Yes
No
35 weeks gestation
FBC, BC, urine and

CSF cultures, CXR
FBC, BC
Adequate IP
CSF suggestive of
meningitis
Observe in hospital
for 48 hours
Yes
Benzylpenicillin
+
Cefotaxime
No
No
Signs of sepsis
at any time
Benzylpenicillin
+
Gentamicin
Yes
Observe in hospital
for 48 hours
ANTIBIOTIC DOSES
Benzylpenicillin 50 mg/kg IV
12 hourly 1st week of life
over 1 week of age
6 hourly
NOTES
The relative risk of EOGBS is significantly greater in preterm neonates than
in babies born at term
Duration of intrapartum prophylaxis (IP) is inversely proportional to the
percentage of babies colonised with GBS
Adequate IP is defined as 2 doses of antibiotics given before delivery
FBC = full blood count; BC = blood culture;
CSF = cerebrospinal fluid; CXR = chest X-ray
Urine must be obtained by suprapubic aspiration or urethral catheter
IP = intrapartum (antibiotic) prophylaxis
Caftriaxone should be avoided in neonates.
38
Cefotaxime 50 mg/kg IV
12 hourly
preterm
8 hourly
1st week of life (term)
6 hourly
over 1 week of age
Gentamicin single daily dose
2.5 mg/kg < 30 weeks gestation
3.5 mg/kg 3035 weeks gestation
5 mg/kg
1st week of life (term)
7.5 mg/kg 1 week10 years of age
T O X O P L A S M A
A L G O R I T H M
Antenatal Evaluation
Routine antenatal screening not
generally recommended in Australia
but is sometimes donea
Serology done because of symptoms

? acute toxoplasmosis: malaise, fever,
lymphadenopathy (eg cervical)
Serology result
IgG ve
IgM -ve
No past infection
Education re: preventionb
Repeat if symptomatic
or routine screeningc
IgG +ve
IgM ve
IgG +ve
IgM +ve
Past infection
No further action
Asymptomatic and
inconsistent/low
+ve IgM
IgA ve and/or
high IgG avidity
Possible recent
infection
Check symptoms and

repeat IgM (different kit)
+/or IgA
+/or IgG titre
+/or IgG avidity d
Negative
Seroconversion
Positive
NOTES
a. Pros & cons of antenatal screening
complex; if it is done, there should be
an appropriate management plan.
b. Avoid raw/undercooked meat; wash
hands after gardening; wash raw
vegetables etc.
c. Various protocols recommend repeat
testing after 1-6 months or at delivery,
to identify seroconversion.
d. IgM can remain +ve for months or
years; IgA, rising IgG level and/or low
IgG avidity are more specific for
"recent" infection (within ~3 months)
Recent toxoplasmosis
definite or probable
ALGORITHM 2
39
Symptoms and/or
additional testing
consistent with recent
toxoplasmosis
Repeated/high +ve IgM
+ve IgA
low IgG avidity
T O X O P L A S M A
A L G O R I T H M
Investigation and Management

of Maternal Toxoplasmosis
Evidence of recent acute maternal
toxoplasmosis (see ALGORITHM 1)
Seroconversion and/or
IgM +ve; IgA +ve; low IgG avidity
symptoms
Risk assessmenta depends on trimester1
Second Trimester:
Fetal infection intermediate risk
(25-40%); if infected, damage
intermediate risk (15-25%)
First Trimester:
Fetal infection low risk (5-15%)a
if infected, damageb high risk
(60-80%)
Third Trimester:
Fetal infection high risk (30-75%)
if infected, damage low risk
(2-10%)
Antibiotic therapy
Consider treatment of mother at diagnosis (depending
on gestation and certainty of diagnosis).
+ve (1st trimester)
consider termination
Intrauterine diagnosis2,3
ultrasonography
amniocentesis d at 18-20 wks gestation or
4 weeks after maternal infection
-ve fetus not

infected; continue
therapyc if maternal
infection fairly certain
NOTES
a. Estimated risks also vary according to the
methods of diagnosis, duration of followup and treatment.
b. Classic signs of congenital toxoplasmosis
are: chorioreinitis; hydrocephalus;
intracranial calcification.
c. Depending on certainty of diagnosis.
Treat with spiramycin (difficult to obtain in
Australia) or
pyrimethamine/sulphadoxine (potentially
toxic in 1st trimester; use with folinic
acid); efficacy of treatment has not been
confirmed in randomised controlled
trials.5,6
d. For PCR and/or culture (sensitivity
~80%); no additional benefit from fetal
blood testing.
e. Neonatal screening and early treatment of
infant is an alternative to antenatal
screening.
+ve (2nd or 3rd trimester)

consider termination if ultrasound
abnormal or
treat mother with sulfadoxine & pyrimethamine (& folinic acid) continuously or
alternating with spiramycin until delivery.
confirm diagnosis in infant
Postnatal investigation and

management of infant at risk
40
Neonatal screeninge4
ALGORITHM 3
T O X O P L A S M A
A L G O R I T H M
Investigation and Management of

Infant at Risk of Toxoplasmosis
Neonatal screen +vea
Full clinical examination

including ophthalmological
and cerebral ultrasound
Maternal infection
treated or untreated
IgM or PCR positive;

+/or infants IgG titre significantly
more than mothers
Investigations:
Infant blood IgM +/or
IgA;4 persistent IgG;
placental
histology/PCR; blood
or CSF PCR
Negative
Clinical and placental

examination normal
& IgM -ve
Symptomatic congenital toxoplasmosis

(minority of infected infantsb)
chorioretinitis/retinal scarring;
intracranial calcification; hydrocephalus;
hepatosplenomegaly; pneumonia;
thrombocytopenia; lymphadenopathy;
myocarditis & IgM +ve +/or abnormal
placenta +/- CSF abnormality (PCR +ve)
Positive result +/or IgG

persists >6 months
Repeat IgG at
6 months of age
Negative
Positive
Infant not infected;

no further action
Asymptomatic congenital toxoplasmosis

(majority of infected infants)
Treatc infant for 12 months with

pyrimethamine & sulphadoxine
(plus folinic acid)
continuously or alternating with spiramycin
(varying combinations used)
NOTES
a. Neonatal screening not often done, but is an alternative to antenatal screening to detect infected infants for treatment.7
b. Proportion of infants infected and severity depends on when maternal infection occurred and if/how treated.
c. High incidence of longterm sequelae (eg chorioretinitis) in untreated infants even if asymptomatic at birth can be reduced by treatment.
41
T R E P O N E M A
PA L L I D U M
A L G O R I T H M
( S Y P H I L I S )
Routine Antenatal Screening

for Syphilis
Non-treponemal screening test
VDRL or RPRa
Positive
Specific treponemal
test e.g. TPPA &/or
FTA-Abs
Positive
High-risk subject
Negative
VDRL &/or RPR titre
Specific treponemal screening test

eg. TPPA, TPHA, syphilis EIA
OR
No
No further
testing
Negative
Positive
Yes
Negative
Repeat at 2832 weeks

gestation and at delivery
VDRL &/or
RPRa titre
& FTA-Abs
Negative
High risk subjectc or symptomatic
Biological
false
positive
VDRL
/RPRb
Both
positive
VDRL
negative FTAAbs positive
Both
negative
? False negative treponemal test

(rarely in very early infection)
Past treated/
latent
infection
Repeat in 4 weeks
Positive
Negative
Biological
false positiveb
False
positive
screening
test
SYPHILIS
Trace sexual contacts

and other children
Perform testing for other sexually

transmitted diseases (including
HIV)
NOTE:
Lettered superscripts refer to notes (see page 44). For reading list, see page 54.
42
Investigate and treat as per

ALGORITHM 2
T R E P O N E M A
PA L L I D U M
A L G O R I T H M
( S Y P H I L I S )
Investigation and Treatment of

Maternal Syphilis
Symptomatic syphilis (rare)
Tissue diagnosis:
(biopsy, exudate etc.)
Darkfield microscopy
Syphilis PCR
Fluorescent treponemal
antibody staining (DFA)h
Rabbit infectivity test
PRIMARY
Ulcer (chancre)
Anogenital
Oral/breast (rare)
Seropositive
Antenatal screening
DETERMINE STAGE
Clinical history/examination
Risk factors sexual contacts, other/previous STDs, IV drug use
SECONDARY
Systemic illness
Fever, rash, hepatitis, lymphadenopathy, meningoencephalitis
LATENT
Asymptomatic
Time since seroconversion (usually not
known): <2 years early; >2 years late
TERTIARY
Cardiovascular
Neurological
Granulomata
? CONGENITAL
Stigmata or
asymptomatic
No risk factors
RISK OF FETAL INFECTION

HIGH
MODERATE
Skin test
Reactive
? Treat
with
cefotaxime
(efficacy
unproven)
Yes
Nonreactive
Desensitise
LOW
NEGLIGIBLE
? Penicillin allergy
Treat with penicillin according to stage

Preferably IM procaine or IV benzylpenicillin
Benzathine penicillin if daily follow-up impossible; crosses
placenta poorly (see Therapeutic Guidelines: Antibiotic)
Repeat VDRL/RPR monthly (or

at delivery)
Negative, low or stationary within

6 months
Neurological signs and

symptoms
Titre persistently
raised >6 months
Lumbar
puncture
CSF
cell count
protein
VDRL &
specific
treponemal
test, PCR
Titre rising near term ?

reinfection
Successful treatment
12 weeks gestation
Successful treatment >12 weeks

gestation to 4 weeks prior to
delivery
Treatment <4 weeks prior to

delivery OR non-penicillin antibiotic
OR benzathine penicillin
Negligible risk of fetal damage
Fetal damage possible
Risk of congenital syphilis
Repeat
treatment
ALGORITHM 3
43
T R E P O N E M A
PA L L I D U M
A L G O R I T H M
( S Y P H I L I S )
Investigation and Management of a

Neonatej Born to a Mother with Syphilis
Mother adequately treated with penicillin (Algorithm 2)
>4 weeks prior to delivery 4 fold decrease in VDRL or
RPR titre (repeat maternal serology at delivery)
Yes
No
Congenital syphilis
possible
Infant unlikely to
be actively infected
Full clinical examination
Normal
Abnormale
Negativef
Positivef
INVESTIGATE
LFT, FBC, UEC; Bone scan
& long bone x-rays; CSFi cell
count, protein, VDRL, PCR, IgM
All investigations
negative
Not infected
Positive
Congenital syphilis symptoms

Abnormal CSF neurosyphilis
Serological follow-up: VDRL/RPR at 1, 2, 4, 6 and

12 months of age or until non-reactive on 2 occasions
Neurosyphilis: repeat CSF examination at 6 months
NOTES
a. VDRL has largely been replaced by RPR (except for CSF
examination). RPR titre is generally higher than VDRL and titres
cannot be directly compared.
b. Biological false positive VDRL/RPR results occur in people with
intercurrent viral and other infections, autoimmune diseases and in
pregnancy.
c. High risk groups: young age, single, low socioeconomic status,
poor education, poor antenatal care, substance abuse, prostitution.
d. Untreated maternal infection in the first trimester is more likely to
produce fetal damage.
e. Clinical abnormalities suggestive of congenital syphilis include rash
(maculopapular or vesicular), mucosal lesions, nasal discharge,
hepatomegaly, bony tenderness and eye lesions. If serology is
negative investigate for other causes.
f. Infant serology negative if VDRL/RPR titre at least four times less
than the mothers and EIA IgM negative; positive if VDRL/RPR
titre at least four times greater than the mothers and/or EIA IgM
Positive
Indeterminatef
Western blot
Benzyl penicillin 50 mg/Kg BD IV 10 days or

Procaine penicillin 50 mg/Kg daily IM 10 days
NO FURTHER
ACTION
Placental histopathology PCRh
Infant serology (VDRL &/or RPR,

EIA IgM)
Negative
g,h
Negative
Congenital syphilis unlikely

Repeat serology at 3 months
& 6 months; treat if serology
positive or follow-up
doubtful
Retreat if persistently
reactive serology, abnormal
CSF or clinical examination
positive; indeterminate if otherwise.

g. Western blot positive if infant serum reacts with additional bands
compared with mothers serum.
h. Western immunoblotting for syphilis antibodies, syphilis PCR and
placental darkfield microscopy, PCR and fluorescent
antitreponemal antibody staining are available as additional
confirmatory tests in reference laboratories.
i. If CSF examination is not possible then give full 10 day penicillin
course and, if possible, perform lumbar puncture at six months to
exclude persistent neurosyphilis.
j. Infants whose mothers develop secondary or early latent syphilis
within 1 year of delivery should be tested and treated if they have
positive serology.
k. The clinical presentation of late congenital syphilis (keratitis,
deafness, Hutchinsons teeth etc.) may be delayed for several
years and regular assessment may be warranted.
l. Serology should be performed on neonatal serum rather than cord
blood because of the risk of contamination with maternal blood.
44
V A R I C E L L A
Z O S T E R
A L G O R I T H M
V I R U S
Exposure to Varicella Zoster Virus

During Pregnancy
Previous maternal
chickenpox
No history or uncertain
past history of chickenpox
Serology not available
Seropositive
Seronegative
No action required
Assess time of exposure
Exposure
< 96 hours
earlier
Exposure
> 96 hours
earlier
Passive immunisation
ZIG
NOTES
Exposure to Varicella or Zoster
for which ZIG is indicated for susceptible persons7
Living in the same household
as a person with active
chickenpox or herpes zoster.
Face-to-face contact with a
case of chickenpox or
uncovered zoster lesions for at
least 5 minutes.
No ZIG
Oral aciclovir if at risk, ie.
Second half of pregnancy1,2,3
Underlying lung disease4
Immunocompromised5
Smoker6
Advise to seek medical attention immediately if chickenpox develops
Remains
well
Develops
chickenpox
45
ALGORITHM 2
V A R I C E L L A
Z O S T E R
A L G O R I T H M
V I R U S
Management of Varicella Zoster

in Pregnancy
Medical review essential if chickenpox
develops during pregnancy
ALGORITHM 1
No complications*
Complications*
or immunocompromised
< 24 hours since

onset of rash
> 24 hours since

onset of rash
Oral aciclovir
No aciclovir
Low risk group

(see Algorithm 1)
Monitor at home
Advise to seek attention
if complications develop
High risk group

(see Algorithm 1)
Complications
develop
Intravenous aciclovir
Supportive therapy
Complications
develop
Monitor in hospital
RECOVERY
NOTES
* Complications:
Respiratory symptoms
Haemorrhagic rash
Persistent fever >6 days
New pocks developing >6
days
Consensus view + refs 1,7-9
(see Appendix 2 for doses)
Fetal medicine counselling
Consider Caesarean section if:

Fetal compromise
Maternal respiratory failure
exacerbated by advanced
pregnancy
ALGORITHM 3
46
ALGORITHM 4
V A R I C E L L A
Z O S T E R
A L G O R I T H M
V I R U S
Fetal Medicine Counselling

Following Varicella Zoster in Pregnancy
Risk of fetal varicella syndrome (FVS)
following maternal chickenpox in pregnancy
Incidence of FVS following varicella in pregnancy
Large case studies suggest rates of

2-2.8% in first 20 weeks gestation10,11
Timing of maternal infection may be important

0.4%
12-20 weeks gestation

2%
>20 weeks gestation Isolated

case reports only
No single diagnostic/prognostic test available

Regular fetal ultrasound for developing anomalies is
recommended12
VZV fetal serology is unhelpful
Consider amniocentesis: ve VZV PCR may be reassuring13
Sequelae of FVS
Frequency10,11
Abnormalities
Skin scars
Eye abnormalities
Limb abnormalities
Prematurity, low birthweight
Cortical atrophy, mental retardation
Poor sphincter control
Early death
47
78%
60%
68%
50%
46%
32%
29%
V A R I C E L L A
Z O S T E R
A L G O R I T H M
V I R U S
Management of Infants from

Mothers with Perinatal Varicella Zoster
Treat infant according to timing
of maternal chickenpox
Maternal chickenpox
> 7 days before delivery
No ZIG required 7
No special interventions
No isolation of infant from
mother
Breast feeding encouraged
Even if baby has chickenpox at
birth or very soon after usually
no interventions are required
unless infant is very preterm*
Maternal chickenpox
7 days before delivery
Very preterm infants born with

chickenpox should receive IV
aciclovir
ZIG required immediately 7,14,15

Should be given < 24 hours
after birth but may be given
up to 72 hours
Discharge term infants as soon
as possible
No other interventions
mother
Maternal chickenpox
028 days after delivery
ZIG required immediately 7,14,15

Should be given < 24 hours
after development of maternal
rash but may be given up to
72 hours
Discharge term infants as soon
as possible
No other interventions
mother
Develops chickenpoxx
*Very preterm infant

in nursery
NOTES
Transplacentally acquired VZV
is high-risk and severity reduced
by ZIG.14,15
Risk also high for seronegative
baby <28 days old.16,17
ZIG not always effective in
preventing severe disease.16,17
See Appendix 2 for aciclovir
dose.
*Very preterm or = 28 weeks
gestation
Term infant at home

or on postnatal ward
IV aciclovir
ALGORITHM 6
Admit to
paediatric unit
Mild disease and ZIG given

< 24 hours after birth
Keep under observation

Treat with IV aciclovir if
respiratory symptoms develop
48
Severe disease or ZIG given

> 24 hours after birth
Treat with IV aciclovir

Supportive care as required
V A R I C E L L A
Z O S T E R
A L G O R I T H M
V I R U S
Management of Term Neonates Exposed to

Varicella Zoster in the Postnatal Wards or at Home
Is exposure significant?
Same open ward as chickenpox case

1 hour or more close contact with staff
member or visitor with chickenpox or
uncovered herpes zoster lesion
No
No
action
required
Note: chickenpox cases may be infectious in 48 hour period

prior to development of rash
Yes
Has mother had chickenpox previously?
Yes
No or Uncertain
Check maternal serology urgently
Seronegative or
serology unavailable
Seropositive
No intervention required
No isolation from affected sibling required
Review if develops chickenpox
Administer ZIG to infant15,16,17

No isolation from sibling required
Medical review if infant develops
chickenpox
Admit to hospital for intravenous aciclovir
if unwell (tachypnoeic, poor feeding)
NOTES
Exposure to Varicella or Zoster considered to be significant within the neonatal unit or postnatal ward.
Patient sharing the same open ward as case of chickenpox or zoster.
Face-to-face contact with a case of chickenpox or uncovered zoster lesions for at least 5 minutes.
Contact for 1 hour or more with case (either staff or patient) with chickenpox lesions or who developed lesions 24 hours later.
49
V A R I C E L L A
Z O S T E R
A L G O R I T H M
V I R U S
Treatment and Isolation of Infants

Exposed to Varicella Within the Neonatal Unit
Is exposure significant?
Same open ward as varicella case

1 hour or more close contact with staff member or visitor with varicella or
uncovered herpes zoster lesion
No
No
action
required
Note: chickenpox cases may be infectious in 48 hour period prior to development of rash
Yes
28 weeks 18
Administer ZIG
Isolate days 7-28 post exposure

Discharge where possible
>28 weeks
Gestational age at delivery
Urgent maternal serology
Seronegative or
serology not available
Seropositive
ZIG
No ZIG


Infant develops varicella
ALGORITHM 4 AND 5
for treatment guidelines
Isolate until all

lesions are crusted
NOTES
Immunisation against VZV of susceptible staff strongly recommended.
APPENDIX 1
Varicella zoster immune globulin
High titre varicella zoster immune globulin (ZIG) is available from the
Red Cross Blood Transfusion Service in Australia on a restricted
basis for the prevention of varicella in high risk subjects. Each vial
contains 2 ml (16% solution of gammaglobulin fraction of human
plasma from donors with high titre of varicella antibodies + thiomersal 0.01% w/v). The recommended dose is 2 ml for children 0-5
years, 4 ml for children 6-12 years and 6 ml for adults.7
Administration is by intramuscular injection with few adverse effects
other than local discomfort reported. This can be lessened if the ZIG
is at room temperature when administered. ZIG should never be
given intravenously.7
Ventilated cases
require strict isolation
Consider transfer out of unit
if isolation cubicle not available
APPENDIX 2
Aciclovir
Aciclovir appears to be a safe and relatively well tolerated drug
although it may impair renal function if given to patients who are not
adequately hydrated.9 It is not licensed for use in pregnancy but
appears to be safe9 and its use is indicated in the high risk situations
outlined.
The recommended intravenous dose for treating VZV infection in
adults and infants is 10-20 mg/kg every 8 hours.
The oral dose for adults is 800 mg five times daily. The use of oral
acyclovir in the neonate is not recommended.
50
R E F E R E N C E S
of infants using HBV vaccine in
Shanghai. Preliminary report of a randomized double-blind placebo-controlled trial. Chin. Med. J. Engl. 1985;
98: 6236
Cytomegalovirus
Acknowledgements
References
A/Professor William Rawlinson (SEALS

Pathology, Virology, Prince of Wales
Hospital, Randwick), and Dr Peter
Robertson (SEALS Pathology, Serology,
Prince of Wales Hospital, Randwick) for
comments on diagnosis.
9. http://www.who.int/vaccinesdiseases/diseases/hepatitis_b.htm
Enterovirus
10. Boxall EH, Flewett TH, Dane DS et al.

Letter: Hepatitis-B surface antigen in
breast milk. Lancet 1974; 2: 10078
Rawlinson WD. Broadsheet. Number

50: Diagnosis of human
cytomegalovirus infection and disease.
Pathology 1999; 31(2): 10915.
2. Lazzarotto T, Spezzacatena P, Pradelli

P et al. Avidity of immunoglobulin G
directed against human
cytomegalovirus during primary and
secondary infections in immunocompetent and immunocompromised subjects.
Clin. Diagn. Lab. Immunol. 1997; 4:
46973.
Further Reading
1. Robath, HA. Antiviral therapy for
enteroviral infections. Ped. Infect. Dis.
J. 1999; 18: 6323
3. Donner C, Liesnard C, Brancart F et al.

Accuracy of amniotic fluid testing before
21 weeks gestation in prenatal diagnosis of congenital cytomegalovirus infection. Prenat.Diagn. 1994; 14: 10559.
2. Sawyer MH. Enteroviral Infections. Ped.

Infect. Dis. J. 1999; 18: 103340
4. Lipitz S, Yagel S, Shalev E et al.

Prenatal diagnosis of fetal primary
cytomegalovirus infection. Obstet.
Gynecol. 1997; 89: 7637.
4. Cherry JD. Enteroviruses. In: Infectious

Diseases of the Newborn Infant. 4th
Edn, 40446. Remington JS, Klein JO,
Eds, WB Saunders & Co., Philadelphia,
1995.
5. Gouarin S, Palmer P, Cointe D, et al.

Congenital HCMV infection: a collaborative and comparative study of virus
detection in amniotic fluid by culture and
by PCR. J Clin Virol. 2001; 2: 47-55.
3. Kearns GL et al. Pleconaril

Pharmacokinetics in Neonates Ped.
Infect. Dis. J. 2000; 19: 8338
5. Rotbart HA, Webster D. Treatment of

potentially life-threatening enterovirus
infections with pleconaril. Clin Infect Dis
2001; 32: 228-35
11. Report of the Committee on Infectious

Diseases, 25th ed. Elk Grove, Ill,
American Academy of Pediatrics, p. 300
Acknowledgements
Dr Joe Sasadeusz at Walter and Eliza Hall
Institute, University of Melbourne and Dr
David McIntosh at Wyeth Vaccines,
Maidenhead, UK
Hepatitis C Virus
References
1. Dore GJ, Kaldor JM, McCaughan GW.
Systematic review of role of polymerase
chain reaction in defining infectiousness
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6. Lazzarotto T, Varani S, Guerra B et al.

Prenatal indicators of congenital
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6. Kearns GL, Bradley JS, Jacobs RF et

al. Single dose pharmacokinetics of pleconaril in neonates. Pediatr Infect Dis J
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7. Hayes K. Cytomegalovirus: The challenge of a common virus infection.

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11. Ivarsson SA, Lernmark B, Svanberg L.
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cover
29/8/05
5:21 PM
Page 1
An infection during pregnancy that could

damage the fetus or infant is much less
common than suspicion or fear of infection.
Vague, nonspecific symptoms malaise,
aches and pains, headache, tiredness, nausea
- are the hallmarks of many vertically
transmissible maternal infections but they are
also common during pregnancy or in any
busy, stressful life. In pregnant women they
cant be dismissed as trivial as they may be in
others.
This publication represents a consensus
among specialists in perinatal infection. It has
been endorsed by the Australasian Society
for Infectious Diseases and the Royal College
of Obstetricians and Gynaecologists of
Australia and New Zealand. We hope it will
not discourage nonspecialists from referring
pregnant women with suspected infection
during pregnancy, but that it will help to guide
the initial assessment and investigation of the
patient, and prevent unnecessary anxiety or
hasty decisions.
Management of
Cytomegalovirus
Enterovirus
Hepatitis B
Hepatitis C
Listeria
Parvovirus
Rubella
Toxoplasma
Edited by Dr Pamela Palasanthiran,

Dr Mike Starr, and Dr Cheryl Jones
Introduction by Prof Lyn Gilbert


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An infection during pregnancy that could

Edited by Dr Pamela Palasanthiran,

AUSTRALASIAN SOCIETY FOR

Edited by Dr Pamela Palasanthiran, Dr

AUSTRALASIAN SOCIETY FOR

Copyright 2002 All rights reserved.

Herpes simplex Virus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16

Human immunodeficiency Virus . . . . . . . . . . . . . . . . . . . . . . . . . 19

Treponema pallidum (Syphilis) . . . . . . . . . . . . . . . . . . . . . . . . . .42

Varicella zoster Virus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45

References and Acknowledgements . . . . . . . . . . . . . . . . . . . . . . 51

Dr Jim Buttery, Paediatric Infectious Diseases, Physician, Royal Childrens

This comprehensive set of contemporary algorithms on the

An infection during pregnancy that could damage the fetus or infant is

There are a few common themes:

Diagnosis of Suspected Maternal CMV Infection

DIRECT VIRUS DETECTION

NOT CMV INFECTION

RECENT PRIMARY INFECTION

COMMENTS: Relevant samples include buffy coat (white

Repeat test 2-4 weeks later

Fetal Risk Assessment

FETAL BLOOD SAMPLING

>20 w (Not performed under 21 weeks)

amniocentesis (for PCR) +/- fetal serology

50% risk of transmissionb

RISK OF SEQUELAE up to 10% e

Risk of fetal morbidity overall is 2025% SEE ALGORITHM 4

Observe mother and infant after birth

If there are clinical concerns, the diagnosis can

SYMPTOMS OF ENTEROVIRAL DISEASE INCLUDE*:

Serology very insensitive, very specific

* peak incidence in the Spring/Summer months in non-tropical or temperate regions of Australia

Intrauterine, perinatal and

Prevention strategies possible

Interpret clinical and

Diagnosis, Management and Follow-up

Nursery epidemics have been controlled

Antenatal Diagnosis of Hepatitis B

All HepBsAg positive

Consider HBV DNA hybridisation

Management of Hepatitis B in Pregnancy

Chronic Hepatitis B infection (HepBsAg+)

Refer for supportive medical management

Hepatitis B: Exposure During Pregnancy

Check serology urgently

Check serology urgently

antiHBs > 10 mIU/mL

antiHBs < 10 mIU/mL

antiHBs > 10 mIU/mL

antiHBs < 10 mIU/mL

Nil further action

At birth: HBIG and HB

Risk vertical transmission:

Management of a mother exposed to HB during pregnancy (see Algorithm 3).

Management of an infant born to a HB carrier mother (see Algorithms 2 & 4):

Revised recommendation for primary HB vaccine schedule for babies

Antenatal Diagnosis of Hepatitis C

All positive Hep C ELISA

Confirm Hep C Ab +ve

All HIV +ve mothers need