Dr.

Putri Mirani, SpOG

Sriwijaya University Faculty of Medicine

 TORCH
- Toxoplasma gondii
- Rubella virus
- Cytomegalovirus
- Herpes simplex virus

Toxoplasmosis
Etiology
Toxoplasma gondii
Transmission
Encysted organism by eating raw or
undercooked beef or pork
Contact with oocytes in infected cat feces

 Fetus can be infected transplacentally

Maternal infection
Symptom:
Fatigue
Muscle pain
Fever
Chills
Maculopapular rash
Lymphadenophathy

 Most often maternal infection is subclinical

Infection in pregnancy abortion or live-born
infant with evidence of the disease
Fetal Effect
Overall < 4th infected newborn with congenital
toxoplasmosis have evidence of clinical illness
Later develop some sequelae of infection

Clinically infected infant at birth:

LBW
Hepatosplenomegaly
Icterus
Anemia
Neurological disease: convulsion, intracranial
calcification, MR, hydrocephaly or microcephaly
Almost all develop chorioretinitis

Management
Routine screening in US not recommended except
pregnant women with HIV infection
Active toxoplasmosis: antimicrobial treatment
recommended
Spiramycin reduces incidence fetal infection but
not modify its severity
Pyrimethamine + sulfadiazine, esp if fetus infected

 Also known as German measles

Etiology: Rubella virus

Tipically cause minor infection in the absence of

pregnancy
Directly responsible for inestimabe wastage as
well as for severe congenital malforations during
pregnancy

Maternal infection
Viremia clinically evident disease 1 week

Disease manifestation:
Lymphadenopathy
Fever
Malaise
Arthralgia
Maculopapular rash begins on the face &
spreads to the trunk & extremities

 Fetal Effects
Advance pregnancy fetal infection are less
likely to cause congenital malformations

Most sequelae seen before 20 weeks

Infant born with congenital rubella shed the
virus for many months threat to other infant as
well as to susceptible adults who come in contact
with them

 The extend rubella syndrome, with progressive

panencephalitis & type 1 DM ay not develop
clinically until the 2nd or 3rd decade of life

1/3 infant who are asymptomatic at birth

developmental injury later in life
Other late sequelae: thyroid dis., ocular damage,
MR

CONGENITAL RUBELLA SYNDROME

Eye lesion: cataracts, glaucoma, micropthalia and other
Heart disease: PDA, septal defects & pulmonary artery
stenosis
Sensorineural deafness
CNS defect: meningoencephalitis
Fetal growth restriction
Throbocytopenia & anemia
Hepatitis, hepatosplenomegaly, jaundice
Chronic diffuse intersitial pneumonitis
Osseus changes
Chromosomal abnoralities

 To eradicated the disease completely it is

recommended to immunizing women in
chilbearing age
Rubella vaccination should be avoided
shortly before or during pregnancy

 DNA herpesvirus that eventuallyi nfects most

human
Most comon cause of perinatal infection
Fetal infection found in 0.5-2% of all newborn
infant
Virus transmitted horizontally by droplet infection
via saliva and urine, vertically from mother to
fetus-infant, can also STD

Maternal infection
No evidence that pregnancy risk or clinical
severity of maternal CMV infection
Most infection are asymptomatic
15% adult have mononucleosis-like synd, ex.
Fever, pharyngitis, lymphadenopathy,
polyarthritis

 Primary infection transmitted to fetus 40%

severe morbidity
Infection during pregnancy are reccurent
Congenital infection from reccurent infection less
often associated with clinically apparent
sequelae than those from primary infections

Congenital Infection
Congenital infection causes cytomegalic
inclusion disease, syndrome that includes:
LBW
Microcephaly
Intracranial calcifications
Chorioretinitis
Mental & motor retardation
Sensorineural deficits
Hepatosplenoegaly, jaundice
Hemolytic anemia & thrombocytopenic purpura

 Diagnosis
Primary infection fourfold-increased IgG titers in
paired acute & convalescent sera simultaneously
OR detecting maternal IgM CMV antibody
Recurrent infection not accompanied by IgM
antibody

In some case effect of fetal infection are

detected by sonography

Management
Currently no effective management for maternal
infection
Serological screening not recommended because
Not possible to predict which fetuses are infected
There is no vaccine
Attempts to identify and isolated infant secreting
CMV expensive & impractical

 VZ-V is a member of DNA herpesvirus family

Almost 95% adults are immune

Primary infection causes chickenpox

Typical maculopapular & vesicular rash
accompanied by constitutional symp & fever for
3-5 days

 Infection in adult tend to be more severe than in

children
Varicella pneumonia is the most serious
complication
Develops in about 10% adults

Treatment for varicella pneumonia: oxygenation,

assisted ventilation acyclovir IV 10mg/kg/8 hours

 Fetal Effects
Maternal chickenpox during first half of
pregnancy may cause congenital malformations
Chorioretinitis, cerebral cortical atrophy,
hydronephrosis, microcephaly, micropthalmia,
dextrocardia, cutaneous and bony leg defects

 No clinical evidence of congenital malformation

with infection after 20 weeks
The highest risk is between 13-20 weeks, with
absolute risk of embryopathy 2%
Fetal exposure just before or during delivery
serious threat to newborn infant

 Management and Prevention

Administration of VZIG prevent or attenuate
infection if given within 96 hours
VZIG dose 125U/kg IM, with max dose 625 units
or 5 vials
Vaccine is not recommended for pregnant
women

 Most common serious liver disease encountered in

pregnant women
At least 5 types: Hep A, B, C, D, E

A sixth agent; Hep. G virus a.k.a GBV-C

In many cases, infection are subclinical

Symptoms ay precede jaundice by 1-2 weeks

Symptoms: nausea, vomitting,headache, malaise and
low-grade fever

 Most fatalities due to fulminant hepatic necrosis

which later in pregnancy must be distinguished
from acute fatty liver

fulminant hepatitis have Hep. B infection

Hepatic encephalopathy fulminant hepatitis
mortality 80%

 Chronic Hepatitis
May lead to cirrhosis and ultimately liver failure
Most cases due to chronic Hep B or C virus
infection
Pregnancy is uncommon when disease is
severe because of anovulation

 There are 4 species of Plasmodium: vivax,

ovale, malariae, falcifarum
Transmitted by the bite of female Anopheles
mosquito
Episodes 3-4-fold during the later two
trimesters of pregnancy and 2 months
postpartum

 Pregnancy enhanced severity of falciparum

malaria, esp nonimmune, nulliparuos women
Insidence of abortion & preterm labor
Stillbirth may caused by plasental & fetal
infection
Neonatal infection is uncommon (7%)

Clinical presentation

Fever & flu-like symptoms

Chills
Headache
Myalgia
Malaise

Symptom may occur at intervals

Symptom less severe in immune patients

 May be asociated with anemia and jaundice

Falcifarum infection kidney failure, coma and
death

Diagnosis
Based on clinical features and identification
intracellular malaria organism on a blood smear

Management
Commonly used antimalarial drugs NOT
contraindicated during pregnancy
Chloroquine is treatment of choice for all forms
of malaria EXCEPT chloroquine resistant
P.falciparum & newly emerging strains of
resistant P.vivax

 Severe malaria chloroquine IV

Woman with chloroquine resistant inf
Mefloquine orally
Severe resistant malaria Quinine or quinidine
IV
Chemoprophylaxis pregnant women traveling
to endemic area

 Prophylaxis initiated 1-2 weeks befor traveling

Chloroquine 300mg of base, PO once a week,
continue until 4 weeks after return to non
endemic areas
Travel to endemic area for chloroquine resistant
discouraged during early pregnancy