SEMINAR

ON

INTRAUTERINE INFECTION
(CONGENITAL INFECTION)
GUIDE: CO-GUIDE:
DR. INDRA BHATI DR. HANSLATA GEHLOT
PRAMOTED BY :
DR. C.P. KACHHAWAHA

PRESENTED BY :
DR. DHARA
DR. S.N. MEDICAL COLLEGE,
UMAID HOSPITAL, JODHPUR (RAJ.)
 INTRAUTERINE INFECTION
Or

(CONGENITAL INFECTION )

Definition: - intrauterine infections are the infections

that occur in fetus during pregnancy & child birth.
Introduction: Fetal infections are an important cause
of mortality & morbidity. Mother may or may not
experience active symptoms of infection during
pregnancy. Infection may occur at any time during
gestation and their severity depending on
1. Virulence of the agent
2. Susceptibility & gestational age of fetus, and
3. Route of infection.
 Most common and important fetal infections may be
Bacterial, Viral and Protozoan
Bacterial agents are
 Group B streptococcal (strep. agalactiae )
 Syphilis
 Escherichia coli
 Staphylococcus aureus
 Klebsiella
 Proteus
 Pseudomonas auraginous
 Listeria
 Tuberculosis
Viral agents are
 Cytomegalovirus
 Rubella
 HIV
 Genital herpes
 Varicella
 Viral hepatitis
 Parvovirus B19 infection
Protozoan agents
 Toxoplasmosis
 Malarial (Plasmodium)
The most serious and most common intrauterine infections,
and the impact of these infections on the mother and infant,
are shortly discussed below.

TORCH INFECTION: TORCH is acronym of

T- Toxoplasma
O- Other infections are
Syphilis

Hepatitis viral infection

Vericella zoster

Parvovirus B19

Listeria

E.coli

GBS infection

R- Rubella
C- Cytomegalovirus infection
H- Herpes simplex virus
 Toxoplasmosis
This is a parasitic infection caused by Toxoplasma gondii.
Most infants are asymptomatic during the neonatal

period but manifestation occurs in 2nd & 3rd decade of life.

Parasite toxoplasma gondii exists in three forms:

The trophozoite (tachyzoite):
 Infect all nucleated cells in the host, replicate, and cause

tissue damage.
The tissue cyst (bradyzoite):
The second form of parasite is formed within host cell as early

as the 8th day of an acute infection and probably persists

through- out the life of the host.
The skeleton, heart muscles, and brain are the most common

sites for latent infection.

The oocyst (sporozoite):
 are produced in the small intestine of cats.
Once shed, the oocyst sporulates in 1-5 days and becomes
infectious, remain infectious for more than 1 year
Route of infection:
Infection occur through mouth by Ingestion of
contaminated raw food, raw or uncooked meat etc.
Tissue cyst and oocyst are resistant to stomach and

small intestine but all forms of the parasite are

destroyed by adequate freezing and heating.

Life cycle:
cat is definitive host in which sexual phase of the
cycle is completed. Oocyst excreted in cat feces.
Contaminated soil ingested by birds, mammals, and

man (intermediate host)

Maternal infection
Maternal infection with toxoplasma is mild or
asymptomatic. Most common clinical signs are
adenopathy and fatigue without fever.
Congenital infection:
Congenital transplacental transmission occurs only
during acute maternal infection.
Vertical transmission is low (15-20%) in first trimester
because placenta act as barrier but foetal damage is
high
While in third trimester infectivity is high (60%) but
foetal damage is less as compare fetal damage occur
in early trimester. i.e. increasing gestational age
increases the fetal infection rate but diminishes
severity.
Rate of infection
1st trimester: 10-15 % but fetal damage is highest
2nd trimester: 25 % but fetal damage is less as compare
3rd trimester: 60 % but fetal damage is lowest

Symptom: Infected infant born with normal

appearance but manifestations occur after several
year of life.

 Chorioretinis – leads to blindness

 Hydrocephalus
 Intracranial calcification shows area of brain damage by
parasite
 Hearing loss (deaf)
 Mental retardation
 Seizure
 Microcephaly
 Hepatoslenomegaly
 Erythroblastosis
The classic triad of congenital toxoplasmosis
 Hydrocephalus
 Chorioretinitis
 Intracranial calcification

Diagnosis: Most commonly used method is antibody detection

Interpretation: IgG(-)
IgM(-) no infection not immune

IgG(+)
IgM(-) infection previous to prenancy

IgG(-)
IgM(+) recent infection. Fetus at risk

IgG(+) acute or chronic infection.

IgM(+) repeat in 2 month
IgM stable---------old infection with persistently raised IgM
IgM to increasing-- infection acquired in the last 2 month fetus at risk
Treatment:
 Aim is to decrease the incidence & severity of congenital infection.
 If IgM positive i.e. acute infection start spiramycin therapy
Spiramycin 1gm for 3 weeks. Stop for 1 wk than restart. 3 cycle.
 Spiramycin delays vertical transmission to fetus
 If intrauterine infection is establishaed pyrimethamine,
sulfonamide, and folinic acid are added.
 Tab pyrimethamine 25mg +sulfadiszine 3 gm for 3weeks.
 Fetal infection diagnosed before 17 wks should be treated with
sulfadiazine alone b/c in first trimester pyrimethamine may affect
organogenesis.

Prevention:
•There is no vaccine for toxoplasma but following measure reduces
congenital infection
• Cook meat to safe temperatures
• Peel or thoroughly wash fruits and vegetables
• Clean cooking surface and utensils that contain raw materials
• Avoid feeding cat's raw or undercooked meat and keep cats indoors
Rubella-:
(German measles) (Rubella is a Grk word that means little red).
This virus typically causes infection of minor import in the
absence of pregnancy.
During pregnancy, however, it has been directly responsible for
abortion and severe congenital malformation.

Causative Agent is Rubella virus (Toga virus)

Wild rubella virus is highly contagious, with only minimal contact necessary for
transmission.
Rubella occurs predominantly in young children, adolescent and most
commonly in springtime.

Maternal manifestations:
Rubella cause fever, malaise, lymphadenopathy, facial rash, postaurical
adenopathy, flu-like symptom, arthralgia and arthritis are characteristic of the
condition.

Immunity: acquired immunity is life long.

Second infections occurring during pregnancy are not associated
with congenital infections
Congenital infection:
Rubella is one of the most teratogenic agent.
If infection occurs before 20 wks of gestation i.e. during organogenesis, child born
with severe congenital malformation known as congenital rubella syndrome.
The possibilities of fetal infection are 61 % when maternal transmissions occur
during the first 4 wks of gestation (post conception weeks).
Possibilities are
61 % at 4 wks
26 % at 5-8 wks
08 % at 9-12 wks
<1 %, after 12 wks
Infection in first week of gestation leads to spontaneous abortion.
Congenital rubella syndrome: it comprises
Auditory manifestation 60-75 % (deafness)
Ophthalmic 50-90 % (blindness)
Cardiac manifestation 40-85 % (PDA)
Cerebral manifestation 25-45 %
Prematuritly
LBW
Neonatal thrombocytopenia
Anemia
Hepatitis
Skin lesion -blueberry manifestation
The extended congenital rubella syndrome:
With progressive pan-encephalitis and type 1 diabetes, may not develop
clinically until the 2nd or 3rd decade of life.
Transmission:
infection can be communicated 7 days before and 4 days after appearance of
rash. Rash occurs 2-3 wks following exposure.
Rash usually last 3 days "3 day measles“
Diagnosis based on IgG & IgM antibodies detection.
Sample may be chorionic villi sampling (CVS), amniotic fluid and fetal blood.
Most common used test is Haemagglutination inhibition test & others are
ELISA, RIA & IFA RT-PCR
Treatment:
There is no specific therapy for either maternal or congenital rubella infection.
Maternal disease is almost always mild and self-limiting.
If primary maternal infection occurs during the first 5 month of pregnancy,
termination option should be discussed with mother.
Treatment of newly born babies is focused on management of the
complications.
Prevention: Rubella is preventable infection.
Rubella vaccine as a part of MMR vaccine must be given to all female children
during childhood.
Conception also should be avoided for 3 month following vaccination.
CYTOMEGALO VIRUS:
 Human herpes virus 5.CMV seed in body
fluid of infected person such as Urine,
Saliva, Blood, Tears, Semen, Breast milk.
 Incidence 0.7-4 % of all pregnancies
complicated by primary infection. Upto 13.5 %
are complicated by recurrent infection.
 Maternal manifestations: Maternal
manifestations are mostly asymptomatic, about
15% develop mononucleosis like syndrome
characterized by fever, pharyngitis,
lymphadenopathy and polyarthritis.
CMV infection in pregnancy leads to congenital
manifestations are
 Pneumonia
 Gastrointestinal manifestation
 Retinal manifestation -blindness
 Neurological disease
 LBW
 Microcephaly
 Hearing loss
 Vision impairment
 Mental retardation
 Thrombocytopenia
 Hepatosplenomegaly
 IUGR
 Non immune hydrops
Ventriculomegaly & calcification in congenital CMV
 CMV tetrad: Mental retardation,Microcephaly,Chorioretinitis

& Cerebral calcification.

 Primary CMV: 30-40 % risk of fetal transmission, 10 % babies born with clinical
signs of infection, 30% with severe infection dies, 80% of survivors have severe
neurological morbidity.
 Recurrent CMV 0.15-2% risk of fetal transmission. Infant are usually
symptomatic. Most common sequelae is isolated hearing loss.
 Diagnosis: detection of IgG & IgM antibodies
 Treatment: No specific treatment or vaccine is available for CMV infection.
 Immunoglobin: Igs should be used as prophylaxis for susceptible women
against primary CMV infection in pregnancy.
 Gancyclovir & Fascornet : These antiviral agents are effective in the treatment
and prophylaxis of the dissemination of CMV in adult immunocomprimised
patient.
 Herpes simplex: two types of virus HSV-1 & HSV-2.
 HSV-1 responsible for the non genital herpes. Genital herpes usually caused
by HSV-2, is sexually transmitted disease that causes painful sore on genitals.
Women who have their first outbreak of genital herpes during pregnancy are
at high risk miscarriage or delivering a low birth weight baby.
 According to American college of Obstetricians and Gynecologists, HSV-2
infections clinically may be divided into three groups:

1. Primary infection is indicated by no prior antibodies to HSV-1 or HSV-2.

2. Nonprimary first episode defines newly acquired HSV-2 infection with

preexisting HSV-1 cross reacting antibodies.

3. Recurrent infection is reactivation of prior HSV-1 or HSV- 2 infection in the

presence of antibodies to the same type of HSV.
 Congenital infection: Majority infections 85% occur during birth .
5% infection occur in intra uterine life. 10% acquired postnataly
 Risk of vertical transmission from mother to fetus

a. 30-60 % if primary genital HSV infection at the time of delivery.

b. 3 % if recurrent genital lesion at delivery

 Symptoms: manifests in 3 form

1. Skin eye mouth herpes (best prognosis) external lesion but no

internal organ involvement. Disease is localized to the skin, eye, or
mucocutaneous membranes. Vesicles typically appear on the 6th to 9th
day of neonatal life. Infants with three or more recurrence of vesicles
have an increased risk of neurological complications.
 2. CNS infection . Herpes infection of brain &
CNS (high morbidity & mortality) presents as
Encephalitis, seizure, lethargy, tremors,
irritibilty, feed poorly, unstable temp. bulged
frontanaele. Symptom develop 10th to 14th
day of life.
3. Disseminated herpes (DIS) infection. Most
severe form of infection with highest mortality.
Affects internal organs as liver lungs
 Other
4. Prematurity
5. Sepsis
 ACOG Recommendation for the HSV infections in the
pregnancy
 Women with active recurrent genital herpes should be offered
suppressive viral therapy at or beyond 36 wks of gestation.
 LSCS delivery is indicated in women with active genital herpes or
prodromal symptoms
 LSCS is not recommended for women with a h/o HSV infection but
no active lesions during labor.
 Routine antepartum genital HSV cultures in asymptomatic patient
not recommended
 Routine HSV screening of pregnant women is not recommended.
 Management: active herpes with a term pregnancy—cesarean
section
 Antiviral agents such as vidarabin & acyclovir should be start at 38
wks of gestation.
 Mother and infant with HSV should be in contact isolation.
 Antiviral agents should be given to infant as per clinical
manifestation.
Other Infection:
 Syphilis: causative agent is Treponema pallidum, a spirochete which is readily
identified by dark field microscopy. Worldwide approximate 1 million pregnancies
are affected by syphilis and 46% of them end up in abortion or perinatal death, 27%
premature and 27%are born with congital syphilis.
 Route of infection: in women syphilis is acquired by sexual contact through small
abrasion on skin and genital mucosa.
 Maternal infection:. There are 30% chance of acquire the disease following
exposure to an infected sexual partner.
 Incubation period is about 3 wks but range is 9-90days. Any stage of infectious
maternal syphilis may result in fetal infection
 Pathological changes in placenta: With
syphilitic infection placenta becomes large
and pale. Microscopically villi appear to have
lost their characteristic arborescent
appearance and to have become thicker and
club shaped. Vessels markedly diminish in
number and in advanced case almost entirely
disappear.
Incidence
Lesions:
 Primary chancre are painless, red, round ulceration
with an indurate base and well formed border and
local painless lymphadenopathy. Frequency of
perinatal transmission is 40-50 %.
 Secondary lesion target like lesions on palmar and
plantar surface are characteristic lesion. Other lesions
are cutaneous rash, mucous patch, codyloma latum
of genitalia, and generalized lymphadenopathy.
Frequency of perinatal transmission is 40-50 %.
 Tertiary lesions involved CNS(neurosyphilis)
cardiovascular system and bones. Frequency of
perinatal transmission is < 10 %
Diagnosis: syphilis cause serological reactions that are used
for confirmation of disease
Non specific
RPR (rapid plasma reagin)
VDRL (venereal disease research laboratory)
Specific reactions
FTA ABS (Fluorescent treponemal antibody absorption test)
MHATP (micro agglutinationassay for antibodies against
T.pallidum)
Congenital syphilis: T. pallidum can cross placenta and cause
congenital fetal infection at any time during pregnancy. Mostly
occur in 4th month of pregnancy. Congenital syphilis is a
multisystem disease. Organism may cause: Stillbirth
Preterm
Growth retardation
Fetal hydrops
Neonatal infection
 Manifestations of Congenital syphilis
 Most of infant look healthy at birth few, has vesicular bullous eruption
usually on palm & sole. From 4 days to 3 wks of life, symptom may
begin and may be grouped as follows:
1. Flu like syndrome
 Meningeal sign
 Lacrimation (iritis)
 Nasal discharge mucous membrane red swollen eroded loaded
with T pallidum
 Sore throat pharynx with mucous patch.
 Generalized arthralgia splinting of arms and legs, osteochondritis
on x-ray film, periostitis particularly tibia (saber sign)
2. Generalized lymphadenopathy
 Cervical, epitrochlear, inguinal, axillary, popliteal
 Hepatoslenomegaly- if severe, probability of aneamia, purpura, jaundice,
edema, hypoalbuminemia
3. Rash
 Maculopapular, postular, and bullous eruptions may all appear together
 Occasionally postular lesions may coalesce to form condyloma latum
Periostitis of long bone in infant Hutchinson teeth in congenital syphilis
Incidence of preterm delivery is 50% in mother with
primary & secondary syphilis, 20% in latent syphilis
and 9% in late syphilis.
Diagnosis based on type of lesions
 By dark field microscopic examination

 VDRL & RPR for screening

 FTA ABS & MHA TP for confirmation

Causes of false positive RPR & VDRL tests are

 Autoimmune disease
 Febrile illness
 Intravenous drug abuse
 Immunization
 Lab. Error
Treatment
 Early latent syphilis: (<1 year) benzathine penicillin
G 2.4 million units IM in single dose
 Late Latent syphilis (>1 year) benzathine penicilline
G 7.2 million units total dose, 2.4 million units IM
each week interval
 Neurosyphilis : procaine penicillion G 7.2 million
units im once daily plus probenecid,500 mg qid
both for 10-14 days.
 Rx of syphilis in penicilline sensitive Pt
Desensitization
Erythromycin 500 mg qid for 15 days
Tetracycline 500 mg qid for 15 days
 Listeria Monocytogenes: gram positive rod shaped
bacteria. Listeria monocytogenes generally occurs in
pregnancy with immunocompromised. Most common
serotype is 1/2a, 1/2b,4b. Listeria monocytogenes is a
intracellular pathogens that commonly occurs in deficit cell
mediated immunity. Because of intracellular it is not
eliminated by antibodies. It cause invasive syndrome such
as
Meningitis
Sepsis
Chorioamnionitis
Stillbirth
IUD
Recurrent abortion
 Rx iv ampicillin, penicillin with amino glycoside.
 Viral Hepatitis: viral hepatitis is an infection that may
have serious implication during pregnancy. There are
atleast five types of viral hepatitis A,B,D, C, & E
 A, C, D, & E –RNA Virus
 B- DNA Virus
 Hepatitis B & C may transmit through placenta to fetus
and cause congenital infection. Hepatitis E is not
transmitting through placenta but cause fulminanat
hepatitis in pregnancy.
 Hepatitis A: is uncommonly diagnosed during pregnancy
because signs & symptoms are unspecific and the
majority of infected individual are asympomatic. The virus
is nonteratogenic and there is no evidence of vertical
transmission. The infection may cause an increased
frequency of preterm birth. The diagnosis is made by
determination of specific antihepatitis a virus IgM.
 Rx Bed rest & supportive therapy.
Adequate nutrition.
 Hepatits B is the cause of 40-45 % of all case of hepatitis
 Incidence 1-2/1000 de novo
 5-15/1000 chronic infection
 Hepatitis B partially double stranded DNA virus. HBsAg is
marker of ongoing HBV infection, its persistency indicates
chronic infection.
 HBeAg is marker of infectivity and viral replication.
 Transmission: highly infectious agent.
 Maternal infections: pregnant women may be affected by
acute HBV infection or chronic infection. Acute infection is
manifestes by Flu like symptoms in 25 % pt., rest are
asymptomatic. 90% of individuals have spontaneous
complete resolution of acute infection, fewer then 1% will die
due to fulminant hepatis and 5-10% become chronic carrier
manifested by continous presence of HbsAg in their serum.
Chronic carrier hepatitis
-70% having chronic persistent hepatitis (disease
does not progress and liver enzyme are normal)
-30% having chronic active hepatitis follow a
different course and frequently develop cirrhosis,
hepatic failure and primary HCC.
Diagnosis based on antigens antibody HBsAg Anti
HBcAg, antiHBsAg liver enzyme will elevated.
Persistency of HBsAg indicate chronic infection.
Presence of HbeAg indicated highly infectious carrier
Screening all pregnant women should be screened
for HBV infection
Screening is usually performed during the first
prenatal checkup time
 Neonatal transmission: most newborns are results of
vertical transmission from chronic carrier or follow acute
infection in last trimester of pregnancy.
 Incidence in 1st & 2nd trimester is 10 %
 when the acute infection occurs in the 3rd trimester, 80-90%
of the new born will be infected. The higher risk of vertical
transmission is from chronic carrier with positive HBeAg.
 Transplacental infection of the fetus is rare and viral DNA
rarely found in the Amniotic fluid and cord blood.
 Most neonatal infection are the result of contact with infected
maternal blood and vaginal secretions during parturition or
acquired during breast feeding.
 Infected new born are usually asymptomatic but if they are
untreated, approximately 85% will developed chronic
infection.
 Breast feeding should be discourage in infant born from
HBsAg positive mother.
 Prevention of Neonatal infection : Can be prevented by
generalized screening of the overall obstetrical population
and administration of hepatitis B Ig and hepatitis B
recombinant vaccine to the new born of women positive for
HBsAg.
 In case of HBsAg positive mother, HBeAg should be done
,if positive than active and passive immunization to baby
should be provided
 Current recommendation is to administer HBV immuno
globulin 0.5 ml im to new born within 12 hrs of Birth
followed by the first dose of hepatitis B vaccine 0.5 ml im
at birth then 1month and 6 month.
 Efficacy of active and passive immunization is 85%-95%.
 Vaccination for HBV infection can be performed during
pregnancy and is Advisable in Sero-negative women at high
risk for infection.
 Hepatitis C it affects 1-5% of all pregnancy and is more
frequent in women with HIV infection.
 Transmission infection acquired through
 infected blood & blood products
 by sexual intercourse
 vertical transmission during pregnancy (3-6%).
 Chronicity is more with hepatitis C infection as compare to
HBV.
 Majority of hepatitis C virus infection are asymptomatic.
 Liver enzymes are elevated and chronicity develop cirrhosis
 Treatment
symptomatic support
in symptomatic patient alpha-interferon and
antiviral ribavirin is benefial
 Malaria: malaria is protozoal parasitic infestation. causative
agent is Plasmodium has four species P. vivex, P.falciparum,
P.malarae, P.ovale
 Route of infection mosquito bite,infected blood
transfusion,transplacental transfer from mother to fetus
during pregnancy.
 P.falciparum is responsible for most of deaths
 Placental parasitization occurs in 15-60%of affected person.
Passive transfer of antibodie to the fetus occur, hence
congenital malaria is rare.
 Maternal manifestation:
Fever -three phage cold, hot, sweating.
Vomiting
Malaise
Headache
Cerebral malaria
 Effects on pregnancy: increased risk of
 Abortion, Preterm, IUGR, IUD, Hyperpyrexia
 Anaemai, Convulsion, Hypoglycemia & Jaundice.

 Complication:
 Hypoglycemia
 Dehydration
 Acidosis
 Anaemia
 Renal failure
 Acute pulmonary oedema
 Coagulopathy
 Convulsion
 Circulatory collapse
 Fluid & electrolyte imbalance
 Jaundice
 & Death.

 M/M: investigation PBF, MP-QBC, PCR

 Rx:- Antimalarial medication
Supportive medication
Nursery care.
 HIV The human immunodeficiency virus is the cause of the
acquired immune deficiency syndrome (AIDS).HIV is infecting
a growing number of women in the reproductive age and as a
consequence the number of infant born to HIV infected
mother is also rapidly increasing.
 There is a significant difference in the incidence, progression
of HIV infection, and use of therapeutic agents between
industrialized and underdeveloped countries.
 There are five type of retroviruses HIV-1, HIV-2, HIV-I, HIV-
II, and HIV-IV, three of them are associated with human
disease. HIV-1, HIV-2 cause of AIDS and HIV-I is also causal
agent of T cell leukemia/lymphoma. Attachment of the virus
to the host cell is a critically important step in the mechanism
of infection.
Individuals at high risk for HIV infection
 Prostitutes (sex worker)

 IV drug abusers

 Women whose partners are

Know HIV positive

IV drug abusers
Hemophiliacs
Homosexual experiences
 Blood transfusion before 1985
Maternal infection
 Maternal HIV is acquired primarily by sexual contact or by
parenteral exposure to infected blood or blood products.
Most sexual transmission is result of receptive vaginal or
anal intercourse with infected partners.
 Most of pregnant women with infection are asymptomatic
in carrier phase.
 Characteristics sign & symptom: generalized lymph node
enlargement, fever, night sweats, weight loss and unusual
recurrent infection such as herpes or candidias.
 Final stage of disease is severe dysfunction of immune
system that is characterized by local infections or
opportunistic infections such as candidias, CMV, herpes,
histoplama, Cryptococcus, pneumocystis carinii develop
Kaposi's sarcoma, lymphoma of the brain or multiple
recurrent bacterial infection.
Fetal transmission:
 Approximately 24% of infants born to HIV infected mother
will demonstrate the presence of the disease by 1 year of
age. The virus is excreted in breast milk and breast feeding
is contraindicated in HIV infected women. In non breast
feeding mother 60-80% of transmission occurs during labor
& delivery & rest during antepartum. Frequency of vertical
transmission increases in relation to the duration of rupture
of membranes and caesarian section is protective.

 The majority of babies born to HIV-positive mothers have

no physical signs of infection. Few of them may exhibit the
HIV embryopathy characterized by Growth retardation,
Microcephaly, and craniofacial abnormalities.
Preventive measure
 1.Detection of HIV infection during pregnancy –screening
test for HIV should be done in 1st ANC visit.

 2.Antepartum care
a. evaluation for other STD
b. serial USG to follow fetal growth
c. weekly nonstrees test after 32 wks
d. measurement of CD4 cells every trimester

I. If CD 4 cell count is greater than 500 regular obstetric

care
II. If CD4 cell count is less than 500, start
azidothymidine(AZT),100 mg five times daily.
III.If CD4 cell less than 200, start prophylaxis for
opportunistic infections.
 3.Intrapartum management
A. If patient not taking any ART agent start ZDV it reduce
frequency of infection to 5-8%.
B. If baby is delivered by LSCS with ZDV neonatal incidence is
2%
C. In the absence of treatment or LSCS incidence of neonatal
infection is about 25%
D. LSCS indicated in case, if >1000 copies/ml viral copy.
E. ZDV-2 mg/kg IV in 1 hrs than 1mg/kg IV infusion till delivery
& to newborn 2 mg/kg oral stat than 1mg/kg 6 hrsly for 6 wks

4. Postpartum care- universal precaution should be continue in

postpartum period. The mother should be instructed to avoid
breast feeding.

5. HAART- highly active antiretroviral therapy.

Group B streptococcal infection (GBS):

 This is a cause of severe congenital infection. A

leading cause of life-threatening perinatal infection.
 15-30% of women are asymptomatic carriers.

Risk factors for infection are

Rupture of membrane for more than18hr.
Preterm delivery
PROM
Multifetal pregnancy
Intrapartum fever
Multiple digital P/V examination during labor
Chorioamnonitis
GBS infection manifests (Clinical manifestation…)
 Stillbirth particularly before 28 wks of gestation
 Infants born with infection manifest as

1 early onset
 Symptoms develop within few hrs (80 % within 6 hrs of delivery) to
first weeks of life, such as
Respiratory distress
Lethargy
Hypotension
Sepsis
 4 % neonatal mortality of term infants and 25 %mortality in preterm
infants.

2 late onset
 symptoms occurs between first weeks to third Week such as

Meningitis is most common

Pneumonia
Sepsis
Maternal manifestation is

 15%-30% women are asymptomatic carriers.

 Asymptomatic bacteriuria
 Chorioamnionitis
 Postpartum endometritis
 Wound infection
 Sepsis

Diagnosis based on

 Culture of sample obtained from lower 1/3 vagina & anorectal

region
 Gram staining
 Other methods are immunofluorescent antibodies, latex
agglutination, colorimetric assays, and enzyme immunoassays PCR.
Preventive measures: Indications are
1. Positive GBS screening during the present pregnancy
2. GBS bactiriuria during the present pregnancy
3. Previous infant with invasive GBS disease
4. Deliveries at < 37 wks
5. Rupture of membrane >18 hrs
6. Intrapartum fever > 38.0c

Universal screening algorithm

 Vaginal and rectal GBS screening cultures at 35-37 wks of

gestation of ALL pregnant women (unless patient had
GBS bacteriuria during the current pregnancy or a
previous infant with invasive GBS disease)
 Intrapartum prophylaxis indicated
• Previous infant with invasive GBS disease
• GBS bacteriuria during current pregnancy
• Positive GBS screening culture during current
pregnancy (unless a planned LSCS, in the absence of
labor or amniotic membrane rupture, is performed)
• Unknown GBS status and of following
- delivery at<37 wks of gestation
- amniotic membrane rupture >18 hrs
- Intrapartum temp. >38.c
Intrapartum prophylaxis not indicated

• Previous pregnancy with a positive GBS

screening culture, unless a culture was also
positive during current pregnancy.

• Planned LSCS, in the absence of labor or amniotic

membrane rupture, is performed regardless of
maternal GBS culture status.

• Negative vaginal and rectal GBS screening culture

in late gestation during the current pregnancy,
regardless of intrapartum risk factors .
Comments on prenatal screening alogrithm
 New recommendation in centers for disease control

and prevention (CDC) guideline:

• Universal prenatal culture based screening for vaginal

and rectal GBS colonization of all pregnant women at
35-37 wks of gestation.

• Updated prophylaxis regimens for women with penicillin

allergy.

• Detailed instruction on prenatal specimen collection

And expanded methods of GBS culture processing,
including instruction on susceptibility testing .
• Recommendation against routine intrapartum
antibiotic prophylaxis for GBS colonized women
under going planned LSCS deliveries who have
not begun labor or rupture of membranes.

• A suggested algorithm for management of

patient with threatened preterm delivery.

• An updated algorithm for management of

newborn exposed to intrapartum antibiotic
prophylaxis.
Recommendation that remain the same

• Penicillin is first line of agent for intrapartum prophylaxis, with

ampicillin an acceptable alternative.
• Women whose culture is are unknown at the time of delivery
should be managed according to the risk approach; the
obstetrics risk factors remain unchanged.
• Women with negative vaginal and rectal GBS screening culture
with in 5 weeks of delivery do not require intra-partum
antimicrobial prophylaxis for the GBS.
• Women with GBS bacteriuria of any concentration during their
current pregnancy or who previously gave birth to an infant with
GBS disease should receive intrapartum anti-microbial
prophylaxes.

• In absence of GBS urinary tract infection antimicrobial agents

should not be used.
Recommend regimens for intrapartum antimicrobial
prophylaxis for GBS infection.

Recommended Penicillin G 5 millions U IV initial dose, then

2.5 millions U every 4 hrs until delivery.
Alternative Ampicillin 2 gm IV initial dose then 1 gm IV
every 8 hrs.
If penicillin allergic Cefozolin 2gm IV then 1 gm IV 8 hrs until
delivery
Or Clindamycin, 900mg IV 8hoursly
Or Erythromycin 500mg every 6hrs
Or Vancomycin 1gm IV BD
For Prophylaxis given IV penicillin 5 mU every 4 hrs until delivery.
Ampicillin 2 gm IV state than 1 gm every 4 hrs until delivery.

Onset of labor or rupture of membrane at <37 wks of gestation with

significant risk for imminent preterm delivery.

No GBS culture GBS culture + GBS culture -

Obtain vaginal & rectal GBS+ Penicillin IV for 48 hrs No GBS

GBS culture & initiate (during tocolysis) prophylaxis
IV penicillin

No growth at 48 hrs IAP AT DELIVERY

Stop penicillin