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1. Teratogenic Maternal
Infection
Maybelle B. Animas

2. • Teratogen is any factor, chemical or physical that
adversely affects the fertilized ovum, embryo or fetus.
FACTORS AFFECTING THE AMOUNT IT CAN CAUSE
• Strength
• Timing- before implantation-zygote is destroyed/appear
unaffected
- 2nd to 8th wks.- very vulnerable to injury
- Last trimester- potential harm decreases
• Teratogens affinity for specific tissue
-Lead- attacks and disables nervous tissue
- Tetracycline- enamel deficiencies, long bone
deformities

4. TORCH
• Group of teratogenic maternal infection which can
involve either sexually transmitted or systemic infection
is described collectively as:
• T- oxoplasmosis
• O- ther disease (Syphilis)
• R- rubella
• C- ytomegalovirus
• H- erpes Simplex

5. • All these infection are known to cross the placenta and
affect the fetus.
• TORCH SCREEN- immunologic survey that determine
whether these infections exist in either the pregnant
women or the newborn.

6. TOXOPLASMOSIS
• Protozoan infection
• Spread commonly through handling cat stool in soil or
cat litter
• Almost no symptoms except for body malaise and
posterior lymphadenopathy
• May cause CNS damage, hydrocephalus, microcephaly,
intracerebral calcification, retinal deformities.

7. Prenatal Diagnosis
• Placental thickening with a “frosted glass”
appearance.
• Cerebral ventricular dilatation, usually
symmetrical and bilateral and leads, to
hydrocephalus
• Hyper-echogenic fetal bowel.
• Hepato-splenomegaly and hepatic
densities, pleural, pericardial effusions
and ascites

8. • If diagnosis is established serum analysis during
pregnancy sulfonamides is precribed
pyrimethamine- antiprotozoal agent
Management
•Remove cat from the home during pregnancy is not
necessary as long as its healthy
•Taking new cat is unwise
•Avoid undercooked meat
•Avoid changing cat litter box or work in soil area whre
cats may defecate.

9. Rubella (German Measles)
• Causes mild rash and mild systemic illness but can bring
devastating effects to the fetus which includes:
– Deafness
– Mental and motor challenges
– Cataracts
– Cardiac defects ( PDA, pulmonary stenosis)
– Retarded IUG
– Thrompocytopenic purpura
– Dental and facial clefts

11. • Rubella virus is transmitted through person-to-person
contact or droplets shed from the respiratory secretions
of infected people.
• Infection can be communicated 7days before and 4 days
after appearance of rash.
• Rash appears 2-3 weeks following exposure & persist
for three days.
• If a woman is infected with rubella virus during
pregnancy, the virus can cross the placenta and
infect the fetus
MODE OF TRANSMISSION
.

12. DIAGNOSIS: Rubella Titer (1st prenatal visit)
– Greater than 1:8- immunity to rubella
– Less than 1:8- susceptible to viral invasion
– Initially extremely high- recent infection has occured
MANAGEMENT
• Woman who is not immunized before pregnancy cannot
be immunized during pregnancy
• After immunization women is advised not to get
pregnant for at least 3 months
• All women with low rubella titer’s should be immunized
to protect against rubella in future pregnancies.

13. CYTOMEGALOVIRUS
• Member of herpes virus
• Transmitted through droplet inection from person-to-
person
• Infant may be born
– Neurologically challenge ( hydrocephalus,
microcephaly)
– Eye damage ( optic atrophy, chorioretinitis)
– Deafness
– Chrionic liver disease
– Blueberry muffin lesions

14. Diagnosis:
• Isolation of CMV antibodies in serum
CMV – PRENATAL USG
Oligo-hydramnios
 Poly-hydroamnios
 IUGR
 Fetal ascites, Hyperechogenic bowel
 Microcephaly, ventriculomegaly
 Intracranial calcification
 Hepatomegaly

15. Prevention
• Thorough handwashing before eating
• Avoid crowds of young children
NO TREATMENT FOR THE INFECTION EXIST.

16. HERPES SIMPLEX VIRUS
• Virus spread into the bloodstream (viremia) and crosses
the to the fetus
• Infection takes place in the 1st tri- spontaneous
miscarriage , severe congenital anomalities
• 2nd or 3rd tri- premature birth, IUGR
• For women with history of genital herpes and existing
genital lesions, CS birth is often advised to reduce the
risk of neonatal infection
• Intravenous or oral acyclovir (Zovirax) can be
administered t women during pregnancy.

17. Syphilis
• Causative agent- Treponema pallidum
• Can extremely damage the fetus after 16th to 18th wk of
intrauterine life
• Transmitted via sexual contact
Diagnosis
– Serologic screening (vdl or plasma reagin)on the 1st
prenatal visit

18. Clinical Manifestations
• Fetal:
– Stillbirth
– Neonatal death
– Hydrops fetalis
• Intrauterine death in 25%
• Perinatal mortality in 25-30% if untreated

19. • Early congenital (typically 1st 5
weeks):
– Cutaneous lesions
(palms/soles)
– HSM
– Jaundice
– Anemia
– Snuffles
– Periostitis and metaphysial
dystrophy
– Funisitis (umbilical cord
vasculitis)

20. • Late congenital:
– Frontal bossing
– Short maxilla
– High palatal arch
– Hutchinson teeth
– 8th nerve deafness
– Saddle nose
– Perioral fissures
• Can be prevented with appropriate
treatment

21. Treatment
• Penicillin G is THE drug of choice for ALL syphilis
infections
• Maternal treatment during pregnancy very effective
(overall 98% success)
• Treat newborn if:
– Mother was treated <4wks before delivery
– Maternal titers do not show adequate response (less
than 4-fold decline)

22. RH SENSITIZATION
• There are blood types A,B,AB,O. Each of these blood
types has specific proteins on the surfaces of their
RBCs. Each of the four blood types is additionally
classified according to the presence of another protein
on the surface of the RBCs (D factor) that indicates the
Rh factor.
• If you carry this protein, you are Rh positive. If you don’t
carry the protein, you are Rh negative.

23. • Rh incompatibility occurs ONLY when an Rh-negative
mother is carrying a fetus with an Rh-positive blood type.
If this occur, the father of the child muat either be
homozygous (DD) or heterozygous (Dd) Rh positive.
• Father is homozygous - 100% the baby will be Rh
positive (Dd)
• Father is heterozygous - 50% the baby will be Rh
positive (Dd)
• When Rh-positive fetus grow inside an Rh-negative
mother, it is as though her body is being invaded bya
foreign agent.

24. • As a result:
– She forms antibodies against invading substance
– Entire RBC is destroyed (Rh factor exist in the RBC).
It crosses the placenta and causes hemolysis.
– Fetus become deficient of oxygen (hemolytic disease
of the newborn or erythroblastosis fetalis).

25. Risk Factors
• Abdominal trauma, such as from a car accident.
• Abdominal surgery, such as a cesarean section.
• Placenta abruptio or placenta previa, both of which can
cause placental bleeding.
• External cephalic version for a breech fetus.
• Obstetric procedures such as amniocentesis, fetal blood
sampling, or chorionic villus sampling (CVS).
• Miscarriage (spontaneous abortion), ectopic pregnancy,
or elective abortion (medical or surgical abortion) after 8
weeks of fetal age (when fetal blood cell production
begins).
• Partial molar pregnancy involving fetal growth beyond 8
weeks.

26. Diagnosis
 All women with Rh-negative blood should have an
anti-D antibody titer done at 1st pregnancy visit.
• result is normal/ titer is minimal (normal is 0,1:8 is
minimal) test will be repeated at 28 wks of
pregnancy. No therepy is needed.
• result is elevated (1:16 or greater) titer should be
monitored approximately every 2wks during the
remainder of pregancy. Amniocentesis is done
every 2wks

27.  Spectrophotometer readings are made (reveal fluid
density)
• Low fluid density (zone1)- no distress, Rh-
negative fetus
• Moderate (zone 2)- preterm birth by induction of
labor at fetal maturity is indicated
• High (zone 3)- immediate birth will be carried out
or IU transfusion begun

28. Management
• RhIG (commercial preparation of passive antibodies
against Rh factor) is administered to women at 28 wks of
pregnancy.
•After birth, infants blood type will be determined by
Coomb’s test.
–If it is Rh-positive/Coomb’s negative, indicating that
a large number of antibodies are not present in the
mother, the mother will recieve RgIG injection.
–If it is Rh-negative baby, no antibodies have been
formed during pregnacy, antibody injection is
unnecessary.

29. Anemia
• Anemia is the common medical disorder during
pregnancy
• Greek meaning “without blood”
• Iron deficiency anaemia is the most common type of
anemia during pregnancy
• 25% direct maternal deaths

30. IRON DEFICIENCY ANEMIA
• occurs as many as 15-20% of all pregnacies
• When the hemoglobin level is below 10mg/dl, IDA is
suspected
• Causes:
Diet low in iron
Heavy menstrual period
Unwise weight reducing programs

31. Characteristic
 Microcytic and hypochromic RBC
 Reduced hemoglobin and hematocrit level (under
33% and 10mg/dl)
 Serum tranferrin- under 100mg/dl
Effects on the baby
 Low birth rate
 Preterm birth
Effects on the mother
 Extreme fatigue
 Poor exercise tolerance

32. Management
 Iron supplement of 60mg as prophylactic therapy
against iron-deficiency anemia
 Advise the women to take supplements with
orange juice or Vit. C supplement
 Eat a diet high in iron and vitamins (green leafy
veg, meat, legumes, fruits)
 Increase roughage in the diet and take pills with
food to avoid constipation and gastric irritation

33. Iron Requirement in Pregnancy
• 2.5mg /day in early pregnancy
• 5.5mg /day from 20 -32 weeks
• 6 – 8 mg/ day after 32 weeks
• Average 4 mg/ day

35. FOLIC ACID DEFICIENCY ANEMIA/ MEGALOBLASTIC
ANEMIA
• Folactin, one of the B vitamins, necessary for formation
of red blood cells in the mother has been associated in
preventing neural tube defects in the fetus
•Seen in 1-5% of pregnancies
•May cause early miscarriage/ premature separation of
the placenta

36. Management
 Women expecting to become pregnant should be
advised to take a vitamin suplement
 Eat folacin rich foods (glv, oranges, dried beans)
 All women of child bearing age should take
supplement of 400ug folic acid daily

37. HYPEREMESIS GRAVIDARUM
• pernicious vomiting
• may result in weight loss; nutritional deficiencies; and
abnormalities in fluids, electrolyte levels, and acid-base
balance.
Factors Causing Hyperemesis Gravidarum
 High levels of hCG (human chorionic gonadotropin).
 Increased estrogen levels.
 Gastrointestinal changes.
 Stress and
 High-fat diet.

38. Distinguishing between Morning Sickness
and Hyperemesis Gravidarum
Morning Sickness Hyperemesis Gravidarum
Appears later than HG and lasts
shorter
Appears earlier and lasts longer
Nausea sometimes accompanied by
vomiting
Nausea accompanied by severe
vomiting
Nausea that subsides at 12 weeks or
soon after
Nausea that does not subside
Vomiting that does not cause severe
dehydration
Vomiting that causes severe
dehydration
Vomiting that allows you to keep some
food down
Vomiting that does not allow you to
keep any food down

39. Management
 A few soda crackers or dry toast when you first
wake up, even before you get out of bed in the
morning.
 A small snack at bedtime and when getting up to
go to the bathroom at night.
 Avoiding large meals; instead, snack as often as
every 1-2 hours during the day and drink plenty of
fluids.
 Eating foods high in protein and complex
carbohydrates, such as peanut butter on apple slices
or celery; nuts; cheese; crackers; milk; cottage
cheese; and yogurt; avoid foods high in fat and salt,
but low in nutrition

40. • Ginger products (proven effective against morning
sickness) such as ginger tea, ginger candy, and
ginger soda. The first used ginger 250mg four times
daily and the second used 1 tablespoon of ginger
syrup in 4-8 fluid ounces of water four times daily.
• Drink and eat little and often.
• Cold meals reduce smell-related nausea.
• Avoid caffeine and alcohol as these can enhance
dehydration

41. EFFECT ON THE FETUS
•Prolonged stress, dehydration and malnutrition during
pregnancy can put the fetus at risk for chronic disease,
such as diabetes or heart disease, later in life, or
neurobehavioral issues from birth.
•Infants born from hyperemetic mother have higher
incidence of low in birth weight

42. ECTOPIC PREGNANCY
• Pregnancy that develops outside a woman's uterus
(womb).
• This happens when the fertilized egg from the ovary
does not implant itself normally in the uterus. Instead,
the egg develops somewhere else in the abdomen. The
products of this conception are abnormal and cannot
develop into fetuses.
• Ectopic pregnancy is usually found in the first 5-10
weeks of pregnancy.

43. PLACE
•The most common place that ectopic pregnancy occurs
is in one of the fallopian tubes.
•Ectopic pregnancies also can be found on the outside of
the uterus, on the ovaries, or attached to the bowel.

44. Common conditions that increase the risk of
ectopic pregnancy include the following:
• Previous tube infections (salpingitis), such as pelvic
inflammatory disease (PID), chlamydia and gonorrhea.
• Previous surgery inside the abdomen, especially
involving the fallopian tubes, ovaries, uterus, lower
abdomen, or bowels
• Use of fertility medications at the time of conception
• The use of an intrauterine device (IUD) does not
increase the risk of ectopic pregnancy. However, a
normal pregnancy is unlikely with an IUD in place, so if a
woman becomes pregnant while using an IUD, it is more
likely the pregnancy is not inside the uterus.
• Prior history of tubal pregnancy

45. Symptoms
• Symptoms of an ectopic pregnancy are often confused
with those of a miscarriage or pelvic inflammatory
disease.
• The most common symptoms are sharp abdominal and
pelvic pain and vaginal bleeding.
• A ruptured ectopic pregnancy is a true medical
emergency.
 Common symptoms of a ruptured ectopic pregnancy
include the following:
 dizziness , pale complexion, sweaty, fast heartbeat
(over 100 beats per minute)
Abdominal or pelvic pain so severe that you can't
even stand up

46. Diagnosis
•An ectopic pregnancy should be considered in any
woman with abdominal pain or vaginal bleeding who has
a positive pregnancy test.
•An ultrasound showing a gestational sac with fetal heart
in the fallopian tube is clear evidence of ectopic
pregnancy.
•An abnormal rise in blood hCG levels may also indicate
an ectopic pregnancy
•A laparoscopy or laparotomy can also be performed to
visually confirm an ectopic pregnancy. A laparoscopy in
very early ectopic pregnancy rarely shows a normal
looking fallopian tube.

47. •A less commonly performed test, a culdocentesis, may
be used to look for internal bleeding. In this test, a
needle is inserted into the space at the very top of the
vagina, behind the uterus and in front of the rectum. Any
blood or fluid found there likely comes from a ruptured
ectopic pregnancy.
•Cullen's sign can indicate a ruptured ectopic pregnancy.
(Cullen's sign is blue-black bruising of the area around
the umbilicus. )

48. Surgery
• Surgery is the final possibility in treatment of an ectopic
pregnancy.
•The therapy for ruptured ectopic pregnancy is
laparoscopy to ligate the bleeding vessels and to remove
ot repair the damaged tube.
Chances of future pregnancy
•The chance of future pregnancy depends on the status
of the adnexa left behind. The chance of recurrent
ectopic pregnancy is about 10% and depends on
whether the affected tube was repaired (salpingostomy)
or removed (salpingectomy).

49. HYDATIDIFORM MOLE
•Gestational trophoblastic disease is the proliferation
and degeneration of the trophoblastic villi.
•As cells degenerate they become filled with fluid appear
to be as grape size vesicles. With this condition embryo
fails to develop beyond a primitive start.
•Mostly likely to occur on women of extreme age
TYPES OF MOLE
–Complete mole
–Partial mole

50. Complete Partial
Trophoblastic Villi
Swell and become cystic Some are form normally
chromosome
46XX or XY (father ONLY) 69 chromosomes
embryo Dies early at only 1-2mm in
size
9wks gestation
HCG Level (both produced
by trophoblastic cells) >50,000 <50,000
Bleeding Vaginal spotting of dark brown blood or profuse fresh blood
accompanied by clear fluid filled vesicle
Human chorionic
gonadotropin (mIU/mL) >50,000 <50,000
Uterine Size
Large for gestation of age
Nause, Vomiting, Hypertension (present before wk 20, No
fetal heart sounds,
Sonogram reveals typically snow flake pattern but no fetal
growth

52. Management
•The primary treatment for hydatidiform mole is suction
D&C.
After the surgical evacuation of a hydatidiform mole,
all patients should be monitored as follows
hCG level should be measured 48 hours after
evacuation.
hCG level should be determined weekly until results
are normal for 3 consecutive weeks, then monthly
until results are normal for 6 to 12 consecutive
months

53. •Pelvic examinations should be performed to monitor the
involution of pelvic structures (e.g., ovaries, uterus) and
to aid in early detection of metastasis.
•Repeat chest radiograph if the hCG titer plateaus or
rises

54. TAPOS NA PO!

55. SAN TAYO KAIN??