I am sharing slide on TORCH infection. I am try my best to cover whole topic up to date.This topic is so lengthy.

1. Fetal Infections
Dr. Jograjiya

2.  T
 O
 R
 C
 H
-TOXOPLASMOSIS
-Others
(Syphilis,VaricellaZoster,ParvovirusB-19,Listerosis,CoxsackieVirus)
-RUBELLA
-CYTOMEGALOVIRUS
-HERPES SIMPLEX VIRUS - 2

3. Mode of transmission in the child
•Placental (chorionic villi)
•Hematogenous (During gestation or at
time of delivery)
TORCH infections can lead to
•Fetal anomalies
•Fetal loss

4. 1. Causative organism
2. Life cycle
3. Mode of infection
1. In mother
2. Fetus
4. Clinical course- in the mother & Fetus
5. Sequel
6. Lab diagnosis
1. Indirect evidences (imp in pregnant women)
2. Direct evidences (imp in fetus infection)
7. Treatment

5. An obligate intracellular parasite.
Human infection is dead end.

6. Definitive host : Felis catus (Domestic cat)
Enteric cycle
 Gametogony and schizogony occurs in the epithelial cells
of Small Intestine.
• Gametogony
ZygoteOocyst
Membrane--Thin
extremely resistant
Cat’s feces
•Unsporulated
•Non infectious
LIFE CYCLE

8. Consists of three forms
 Tachyzoites
 rapidly multiplying forms,
 invade & multiply within cells
 Silver stains used to detect
 Bradyzoites
 slowly multiplying forms
 Present inside tissue cysts
 PAS positive
 Sporozoites
 inside oocysts, shed in feces of cat and remian in the environment

9. MODE OF INFECTION:
 Infective form : Sporulated Oocyst containing sporozoites
• Ingestion of Sporulated oocysts ( raw meat and vegetables)
• Contact with oocysts in cats’ feces/contaminated soil
• Transfusion of infected blood
 The incidence during pregnancy ranges from 0.3-1 %
• Of these 1 in 10 will deliver a baby with congenital Toxoplasmosis
Ingestion
Contact
 Transfusion

11.  Sporozoites penetrate epithelium of ileum
Sporozoites Ileum
Mesenteric
LN
Blood & Lymph
stream
Distant
organs
2. Tissue cyst/ extracellular form
•Brain, Skeletal muscle
•Has cystozoite
Lodgement is in two forms
1. Pseudocyst/intracellular form
(proliferative stage).
•Cells of R.E. System, Placenta.
•Has a crescent shaped endozoite of
6µ by 2µ

12. CLINICAL FEATURES
•Only 10% have a symptomatic illness.
•Painless lymphadenopathy is the most common
presenting feature. Cervical lymph nodes most
commonly.
The mesenteric, mediastinal or the
retroperitoneal nodes may also be involved.
•Other features include – Malaise, Fever, Fatigue,
Muscle pain, Sore throat and headache.
• Most pregnant women ( > 90%) remain
asymptomatic and spontaneous recovery is the
rule.

13. •Complete resolution occurs within
a few months, although some
patients do not recover
completely even for a year or
more.
•In immunocompromised pregnant
women, may also develop
encephalitis, hepatitis, pneumonitis
and myocarditis.

14. CONGENITAL TOXOPLASMOSI
The risk of vertical transmission increases with
gestational age, with the highest rates (60%
to 81%) in the third trimester compared with
6% in the first trimester.
Disease severity, however, decreases with
gestational age, first trimester 80%
developing symptoms or major sequelae
while 5% perinatal mortality while in third
trimester 10% and 0% respectively.

16. Congenital toxoplasmosis is characterized
by the tetrad (Sabin in 1942)
 Chorioretinitis 86%
 Intracranial calcification 37%
 Hydrocephalus 20%
 Convulsion 1-2%

17. SEQUELAE
If fetus develops sub clinical infection -
 Asymptomatic at birth .
 Later on develops
• Mental retardation AND Learning difficulties
• Cerebral calcifications
• Chorioretinitis blindness
• Hydrocephalus
• Epilepsy.

18.  Indirect evidences
• Antibody demonstration
 Direct evidences
• Staining
• Microscopy
 Prenatal diagnosis
• Done when IgM & IgG positive with low avidity

19. Antibody demonstration (Screening tests)
 ELISA METHOD.
 Indirect immunofluorescence test (sabin-feldmen dye test).
 Goldman’s test ( fluorescent tagged Ab.)
 Fulton’s agglutination Test.
 Complement Fixation Test.

20. ELISA- Routinely used
 For IgM and IgG antibodies
 IgM- Detection of specific IgM antibodies
 IgG Assays include
1. Detection of specific IgG antibodies
2. IgG Avidity testing

21. IgG IgM INTERPRETATION FOLLOW UP TESTING
Negative Negative
Negative
Positive/
equivocal
Positive Negative
Positive Positive
No serologic evidence of T.
gondii infection
• acute T. gondii infection
• False +ve IgM reaction
Obtain a new specimen for IgG and IgM testing or
retest this specimen using a different assayAll Indeterminate results
further testing in a reference laboratory
for the diagnosis of toxoplasmosis.
T. gondii inf. within past 1 yr or
false +ve IgM reaction.
Infected with T. gondii for more
than 1 year.
second specimen aft 2-3 weeks for IgG
and IgM testing; if same results, then its
false +ve IgM reaction
No follow up testing required

22. Live Tachyzoites + Accessory factor + Test serum (Serial dilutions)
Incubation at 37° C for 1 hour
Alc. soln of Meth. Blue (pH-11) Examine under 40x

23.  Highest dilution for which <50% of free toxoplasma
have stained cytoplasm is taken as titre.
 Titres of 1:128- diagnosis of acute inf.

24. Microscopy :
 Tachyzoites in smears of lymph
nodes, brain, bone marrow .
Stain : PAS- Bradyzoites
Wright’s Giemsa- Tachyzoites
Presence of tachyzoites in clusters : Acute infection
DIRECT EVIDENCES - CONFIRMATORY TESTS

26. Toxoplasma specific IgG
IgG NEGATIVE IgG POSITIVE
IgG +ve, IgM -ve
NONIMMUNE
susceptible
Test for Toxo. SPECIFIC IgM ANTIBODY
IMMUNE INFECTED FOR > 1 year IgG AVIDITY
Low IgG Avidity HIgh IgG Avidity
OLD INFECTION
16wks – 1 yr
RECENT INFECTION < 16WKS
Repeat test after 2 wks to confirm before
intervention
IgG & IgM POSITIVE

27.  Amniocentesis –
amniotic fluid PCR for
parasite particles.
sensitivity 81% to 90%,
specificity 96% to 100%.
 Placental tissue / Blood –
inoculation into mice &
isolation of parasites
 USG

28.  Anomaly of CNS –Ventriculomegaly, calcifications in
the brain parenchyma, periventricular zone and
caudothalamic zone, periventricular echogenicity or
cyst.
 Cataract
 IUGR
 Hepatomegaly, Liver calcification, Ascites.
 Placental enlargement /thickening.

29. 1. Routine universal screening should not be
performed for at low risk and offered only to at risk
for primary Toxoplasma gondii infection. (II-3E)
2. Suspected recent infection should be confirmed
before intervention. (II-2B)
 3. If acute infection is suspected, repeat testing should
be performed within 2 to 3 weeks, and consideration
given to starting therapy with spiramycin immediately,
without waiting for the repeat test results. (II-2B)

30. 4. Amniocentesis should be offered
• (a) if maternal primary infection is diagnosed,
• (b) if serologic testing cannot confirm or exclude acute
infection, or
• (c) in the presence of intracranial calcification, microcephaly,
hydrocephalus, ascites, hepatosplenomegaly, or severe
intrauterine growth restriction in USG. (II-2B)
5. Amniocentesis should not be offered at less than
18 weeks’ gestation and should be offered no less
than 4 weeks after suspected acute maternal
infection to lower the occurrence of false-negative
results. (II-2D)

31. Indication Treatment
only IgG positive No treatment
If maternal infection has occurred but
the fetus is not infected
SPIRAMYCIN 1 g (3 million U) orally every 8 hours should be
given until term if the amniotic fluid polymerase chain reaction is
reported negative for T. gondii.
Reduced the rate of vertical transmission 60%.
If evidence of fetal infection
1. Amniotic fluid PCR positive
2. Ultrasound signs
1. pyrimethamine 50 mg or 1 mg/kg q 12 hours for 48 hours as
a loading dose, 50 mg or 1 mg/kg per day, plus sulfadiazine
75 mg/kg, followed by 50 mg/kg q 12 hourly, plus folinic acid
(leucovorin) 5-25 mg with each dose of pyrimethamine; is
recommended as SPIRAMYCIN does not cross the placental
barrier.
2. consider MTP before 20 weeks of gestation

32.  Wear gloves and thoroughly clean hands and nails when handling material
potentially contaminated by cat feces (sand, soil, gardening).
 Reduce the exposure risk of pet cats by (1) keeping all cats indoors (2)
giving domestic cats only cooked, preserved, or dry food.
 Change litter and get rid of cat feces (wearing gloves) on a regular basis
(every 24 hours).
 Disinfect emptied cat litter tray with near-boiling water for 5 minutes before
refilling.
 Eat only well-cooked meat ( > 67°C/153°F).
 Freezing meat to at least −20°C/−4°F also kills T. gondii cysts.
 Clean surfaces and utensils that have been in contact with raw meat.
 Do not consume raw eggs or raw milk.
 Wash uncooked fruits and vegetables before consumption.
 Prevent cross-contamination: thoroughly clean hands and utensils after
touching raw meat or vegetables.
 Do not drink water potentially contaminated with oocysts.
 Be aware that
• the process of curing, smoking, or drying meat does not necessary result in a product
free of parasite cysts.
• refrigeration does not destroy the parasite (still viable after 68 days at +4°C).
• microwave oven cooking does not destroy parasites.

33. 6. Toxoplasma gondii infection should be suspected
and screening should be offered to pregnant women
with intracranial calcification, microcephaly,
hydrocephalus, ascites, hepatosplenomegaly, or
severe intrauterine growth restriction in USG. (II-2B)
7. Each case suspected of having an acute
Toxoplasma gondii infection acquired during
gestation should be discussed with an expert in the
management of toxoplasmosis. (III-B)

34.  8. If maternal infection has been confirmed but the fetus
is not yet known to be infected, spiramycin should be
offered for fetal prophylaxis (to prevent spread of
organisms across the placenta from mother to fetus). (I-
B)
 9. A combination of pyrimethamine, sulfadiazine, and
folinic acid should be offered as treatment for women in
whom fetal infection has been confirmed or is highly
suspected (usually by a positive amniotic fluid
polymerase chain reaction). (I-B)
 10. Anti-toxoplasma treatment in immunocompetent
pregnant women with previous infection with
Toxoplasma gondii should not be necessary. (I-E)

35. 11. Women who are immunosuppressed or HIV-
positive should be offered screening because of the
risk of reactivation and toxoplasmosis encephalitis.
(I-A)
12. A non-pregnant woman who has been
diagnosed with an acute Toxoplasma gondii
infection should be counselled to wait 6 months
before attempting to become pregnant. (III-B)
13. Information on prevention of Toxoplasma gondii
infection in pregnancy should be made available to
all women who are pregnant or planning a
pregnancy. (III-C)

36. • VARICELLA ZOSTER
• PARVOVIRUS B-19 INFECTION
• SYPHILIS
• COXSACKIE VIRUS INFECTION
• LISTEROSIS

37. •A member of the herpes virus family.
•The acute primary infection cause Chickenpox.
It is a highly contagious systemic disease that normally
results in lifelong immunity.
•The virus may persist in a latent state in the posterior
root ganglia of the spinal cord for year.
• Reactivation results in Herpes Zoster.
•Incubation Period – 15 days and is communicable 2
days before and 5 days after the onset of rash.

38. Transmission
• Droplet spread when a person with chickenpox coughs
or sneezes.
• Direct contact with upper respiratory secretions or with
lesions that have not yet crusted.
•Airborne spread, which is more likely in
immunocompromised individuals.
• Congenital vertical transmission.
It is usually acquired by 90% of the population before
the reproductive age, thus most women are immune
before they become pregnant.
The incidence is 0.7/1000.

39. Vesicular eruptions often on mucosal
surfaces first followed by a rapid
dissemination in a centripetal pattern.
New lesions appear every 2-4 days and
each crop is associated with fever.
The rash progresses from macules to
vesicles and then to pustule in 24 hours.

41. •Maternal varicella infection in
pregnancy can cause VARICELLA
the first 20 weeks of
EMBRYOPATHY.
Congenital Varicella Syndrome (1-2%)
characterized by IUGR, hallmark cicatricial
lesions in dermatomal pattern, limb hypoplasia,
contractures and involve the eye and central
nervous system.
The prognosis is poor if an infant be infected.
•However, the risk of congenital varicella
syndrome is negligible because antibodies in
the maternal blood prevent the virus from
crossing the placenta and infecting the fetus.

42.  Anomaly of CNS –Ventriculomegaly, Microcephaly, intra-
cranial calcifications, cerebral hypoplasia, Porencephaly
 Microphthalmia, cataract
 IUGR
 Limbhypoplasia
 Skeletal abnormalities
 Placental anomalies
 Hydrops fetalis
 Cutaneous scaring, Mandelbrot L

44. DIAGNOSIS :
Is primarily clinical, by recognition of the rash. If necessary,
it can be confirmed by detection of
Immunofluorescence), PCR or by
VIRAL aspirated Vesicular Fluid.
antigen (Direct
CULTURE of the
TREATMENT :
ACYCLOVIR (800mg 5 times daily at 4 hourly intervals for 5
days) or ACYCLOVIR 5mg/kg 8 hourly IV until patient is
improving is a Class-C antiviral agent used in the treatment
of Varicella Zoster. Oral Acyclovir has been shown to
significantly reduce symptoms, duration and intensity.
•Many studies have showed the safety of Acyclovir use in pregnancy. In 1993,
Center for Disease Control published data showing no risk of fetal
abnormalities in patients exposed in the first trimester receiving Acyclovir.
•The newer drugs like VALACYCLOVIR and FAMCYCLOVIR have a better bio-availability
and a less frequent dosing than Acyclovir with similar efficacy.

45. PARVOVIRUS B-19 INFECTION :
A small single stranded DNA virus and has
a predilection for rapidly dividing cells
particularly the erythroblasts.
Many infections are sub- clinical.
•Incubation Period – 14-21 days.

46.  Epidemic trend occur to every 4 years with yearly peak of
incidence in spring.
 Maternal infection occur through
• Respiratory droplets
• Transfusion
 Maternal viraemia after 7 days
 IgM detected between 7-14 days
 IgG detected between 14-21 days

47. Most asymptomatic
Mild fever , headache, Arthralgia and
erythema infetiosum
Pregnant women with immune-compromised
or preexisting hematological disease more
likely to develop transient aplastic crisis lead
to morbidity and mortality of mother.

49.  MOT- Transplacentally
 No vertical transmission if the mother is immune at time
of exposure.
 Transmission rate 30-50%
 Affection rate 10%
 It causes Miscarriage, IUGR, Fetal anemia, Non-
immune hydrops fetalis and rarely thrombocytopenia.
 It may directly affect myocardium, which can cause
arrhythmias or even cardiac failure and periventricular
calcification involving cortex, basal ganglia and thalami.

52. Serological examination of maternal blood
IgM detectable b/w 7-14 days, peak at 10-14 days,
decrease within 2-3 months.
IgG produced during 14-21 days.
Window period 7days.
The rapid fall in IgM concentration usauly 2 or 3 month
give false negative value.
In this case sign of infection in USG or PCR of maternal
blood may help in diagnosis.

53. It can be identified histologically by characteristic
intranuclear inclusions or by the presence of viral
particles by electron microscopy (Levy et al., 1997).
Viral DNA may also be identified by PCR of
amniotic fluid or fetal blood by cordocentesis.
Amniocentesis, invasive diagnosis of this condition
is not required for all suspected or confirmed
maternal infections because non invasive USG is
available.

54.  Increased nuchal translucency
 Abnormal ductus venosus
 Suspect fetal anemia due to PB19 infection if following
• An increased peak systolic velocity in MCA
• Mother is RH+
• Or in contact with suspected PB19 infection.
 In high-output cardiac failure and fetal hydrops
• Cardiomegaly
• Pericardial and pleural effusion
• Ascites
• Skin edema
• Placentomegaly
• Polyhydromios

55. No specific antiviral therapy and vaccine is available.
If a recent infection, the virus may be transmitted to the
fetus (17 to 33%) and may cause nonimmune hydrops.
 Sign of fetal anemia, high-output cardiac failure and
hydrops monitor by UGS,
• Within 4 weeks after maternal infection if negative then
• F/U scan every 1 or 2 weeks.
• If no fetal abnormality at 30 weeks, mother can be reassured.
 If in scan sign of anemia or overt hydrops fetalis the
patient should be referred to higher center where
intrauterine transfusion available.

57. SYPHILIS
•Syphilis is caused by infection, through abrasions
in the skin or mucous membranes with the
spirochete TREPONEMA PALLIDUM.
•In adults the infection is usually sexually
acquired, however transmission by kissing,
blood transfusion and percutaneous injury have
also been reported.
•Infection may remain latent throughout or
clinical features may develop at any time.

58. •Syphilis may be divided as Early or Latent Syphilis.
•CLINICAL FEATURES :
• Incubation period of Early Syphilis is usually 14-28 days
with a wide range of 9-90 days.
•The primary lesion or chancre develops at the site of
infection usually on the genital area and may also develop on
the vaginal wall and the cervix.
•After 6-8 weeks the treponemes disseminate to produce a
multi-system disease. Constitutional features such as fever,
malaise and headache are common. Over 75% patients
present with a rash on the trunk and limbs that later
involves the palms and soles.
•Generalised non-tender lymphadenopathy is present in over
50% patients.

59. CONGENITAL SYPHILIS
• Is rare where antenatal serological screening is
practiced.
•A variety of outcomes after 4 months of gestation when
the fetus becomes immunocompetent:
1. Miscarriage or Still-birth, Premature or at term.
3. Birth of a baby with latent infection who either remains
well or develops Congenital Syphilis later in life.
2. Birth of a syphilitic baby (very sick baby with
hepatosplenomegaly, bullous rash and perhaps
pneumonia).

60.  IUGR
 Hydrops, ascites, pleural and pericardial effusion,
generalized skin edema.
 Hyper-echogenic bowel, Liver calcification.
 Hepato-splenomegaly.
 Placental thickening.
 Shortening of long bone.
 Bone deformity (bowing, curvature and thickening)

61. •Often features such as meningitis, cranial nerve palsies,
hepatitis, gastritis, glomerulonephritis and anterior/posterior
uveitis are seen.
INVESTIGATIONS :
SEROLOGICAL TESTS FOR SYPHILIS
Non-treponemal ( Non-specific) tests:
•Veneral Diseases Research Laboratory ( VDRL ) Test
•Rapid Plasma Reagin Test
Treponemal (Specific) antibody tests:
•Treponemal antigen-based enzyme immuno assay
(EIA) for IgG and IgM
•T. Pallidum haemagglutination assay (TPHA)
•T. Pallidum Particle agglutination assay (TPPA)
•Fluorescent treponemal antibody-absorbed (FTA-
ABS) test

63. TREATMENT :
 Untreated early syphilis, 70-100% of infants will
be infected, with stillbirths in up to one-third of
cases.
 Most transmissions to the fetus occur after 20
weeks and treatment before this period will
usually prevent congenital features.

64. Benzathine penicillin G (BPG) 2.4 million units IM
single dose (or 1.2 million units in each buttock) [I;
B]
Replacing part (i.e. 0.5 to 1cc) of the solvent by
lidocaine 1% solution without epinephrine may
reduce the discomfort associated with injection.
This is not possible in case of pre-mounted
syringes.
Patients should be kept for 30 min clinical
surveillance after injection.
Note: some specialists recommend 2 doses of BPG 2.4 million units (day 1
and 8) but this is not sufficiently evidence based.

65. Procaine penicillin 600,000 units IM daily for 10-14
days, i.e. if BPG is not available [III; B]

66.  Benzathine penicillin G (BPG) 2.4 million units IM (one
injection 2.4 million units single dose or 1.2 million units
in each buttock) weekly on day 1, 8 and 15 [III; B]
 Replacing part (i.e. 0.5 to 1cc) of the solvent by
lidocaine 1% solution without epinephrine may reduce
the discomfort associated with injection. This is not
possible in case of pre-mounted syringes.
 Patients should be kept for 30 min clinical surveillance
after injection.

67. All pregnant women should be screened at first
antenatal visit (first trimester).
Serology should be repeated at 28-30 weeks in
case of high risk and local epidemiology.
Some specialists recommend that all infants born to
syphilis seropositive mothers should be treated with
a single dose of BPG 50,000 units/kg IM, whether or
not the mother was treated during pregnancy.

68. T. pallidum demonstrated by Dark field examination
or polymerase chain reaction in placenta or
autopsy material, exudate from suspicious lesions
or body fluids, e.g. nasal discharge.

69.  Interstitial keratitis, Clutton's joints, Hutchinson's
incisors, mulberry molars, high palatal arch, rhagades,
deafness, frontal bossing, short maxilla, protuberance
of mandible, saddlenose deformity, sterno-clavicular
thickening, paroxysmal cold haemoglobinuria,
neurological or gummatous involvement.
 Serological tests can be negative in infants infected in
late pregnancy and should be repeated. When the
mother is treated during the last trimester of pregnancy,
the treatment can be inadequate for the child and the
child may still develop congenital syphilis.

70. RPR/VDRL, TPPA/TPHA (quantitative), anti-
treponemal IgM-EIA, treponemal IgM – from infant’s
blood and not umbilical cord blood, because false-
positive and false-negative tests may result.
Blood: Full blood count, liver function, electrolytes
CSF: cells, protein, RPR/VDRL, TPHA/TPPA
X-rays long bones
Ophthalmic assessment as indicated

71. Benzyl penicillin 150,000 units/kg IV daily
(administered in 6 doses every 4 hours) during 10-
14 days [IV; C]
If CSF is normal: check for age
1. First line therapy: BPG 50,000 units/kg IM (single dose) up
to the adult dose of 2.4 million units [IV; C]
2. Second line therapy: Procaine penicillin 50,000 units/kg IM
daily for 10-14 days, i.e. if BPG is not available [IV; C]

72. Procain penicillin G, 2.4 million units IM once daily
plus Probnecid, 500 mg orally four times daily, both
for 10-14 days.
OR
Aqueous crystalline penicillin G, 18-24 million units
per day, administered as 3-4 million units IV every 4
hours or continiuors infusion for 10-14 days.

73.  An acute febrile illness with headache, myalgia, chills and
rigors, resolving within 24 hours.
 Common in early syphilis also neurological or ophthalmic
involvement, in neonates or in pregnancy when it may cause
fetal distress and premature labour.
 Uncommon in late syphilis but can potentially be life
threatening if involvement of strategic sites (e.g. coronary
ostia, larynx, nervous system).
 Management:
1. If cardiovascular or neurological involvement (including optic neuritis)
exists, inpatient management is advisable.
2. Prevention of Jarisch-Herxheimer reaction: Prednisolone 20-60 mg daily
for 3 days, starting anti-treponemal treatment after 24 hours of
commencing prednisolone [IV; C]
3. Antipyretics
Jarisch-Herxheimer reaction

74. Due to accidental IV injection of procaine penicillin
and may be minimized by the "aspiration technique"
of injection.
Characterised by fear of impending death, may
cause hallucinations or fits immediately after
injection. Lasts less than 20 minutes.
Management:
1. Exclude anaphylaxis
2. Calm and verbal reassurance; restraint may be necessary.
3. Diazepam 5-10 mg rectally/IV/IM if convulsions

75. Facilities for treatment of anaphylaxis
should be available as penicillin is one of
the most frequent causes.
Management:
• Epinephrine (adrenaline) 1:1000 IM 0.5 ml
followed by:
1. IM/IV antihistamine e.g. chlorpheniramine 10 mg
2. IM/IV hydrocortisone 100 mg

76. COXSACKIE VIRUS INFECTION
•The virus is a member of the Picornaviridae and have a
single-stranded RNA.
•It may cause clinically inapparent infection in the
mother but may prove fatal to the fetus or the infant by
increasing congenital malformations.
•Infection is spread from person to person. The virus is
present in secretions and body fluids of infected people.
•Fetal death may be caused by viraemia resulting in
Hepatitis, Myocarditis and Encephalomyelitis due to
placentitis and clinical chorioamnionitis.
•The virus may be grown from the amniotic fluid or the
neonatal spinal fluid.PCR can detect 66-90% of the
infection.

77. CLINICAL FEATURES : Common Cold, Rash, diarrhoea,
meningitis,sore throat. Severe manifestations include
encephalitis, severe chest pain, myopericarditis.
TREATMENT :
•There is no specific
Coxsackie virus.
medication known to kill the
•Fortunately, the body’s immune system is usually able to
destroy the virus.
•Some reports suggest that there might be a benefit to IV
Immunoglobulin which is made from human serum and
contains antibodies.
•Treatment for Myocarditis is supportive.

79. LISTEROSIS :
•Recent surveys have shown that 4% of pregnant women
harbor LISTERIA MONOCYTOGENS, a Gram-positive
bacteria in the cervix.
•Trancplacental infections can occur from an infected
mother.
•Such patients have Influenza like symptoms, premature
delivery and dirty brown amniotic fluid, fever, myalgia,
choriamnionitis and abortions.
and mortality due to Pyogenic Meningitis.
•Babies born to these mothers may get infected
transplacentally or during delivery with a high morbidity

80. INVESTIGATIONS :
•Diagnosis is made by Blood/CSF Culture, a positive
fluoroscent antibody test and culture of stomach content,
liquor .
TREATMENT :
•The most effective regimen consists of IV AMINOPENICILLIN
(AMOXYCILLIN/AMPICILLIN) + AN AMINOGLYCOSIDE.
•Patients allergic to Penicillin may be given a combination
of Sulfamethoxazole/Trimethoprim.
•Dietary precaution : Pregnant women are advised to
avoid high-risk products like undercooked chicken, fish, raw
vegetables and soft cheese.

81.  Rubella, caused by the rubella virus.
 Minor infection in absence of pregnancy.
 But during early pregnancy it is directly responsible for
abortion and severe congenital malformations to fetus.
 Acquired immunity is life long.
 It is Vaccine-preventable disease.

82. Properties
Family- Togaviridae
Genus- Rubivirus
Pleomorphic, roughly spherical.
50-70nm in diameter
ssRNA genome
Enveloped with haemagglutinin polymers.

83. MODE OF TRANSMISSION
• Person to person contact
• Droplet secretions of the infected.
 Rash appears 2-3 weeks following exposure & persist for
three days.
 Infection can be communicated 7days before and 4 days
after appearance of rash
Transmission to fetus- transplacental

84. CLINICAL FEATURES :
•German measles causes symptoms that are similar to the
flu. The primary symptom of rubella virus infection is the
appearance of a rash (exanthem) on the face which
spreads to the trunk and limbs and usually fades after three
days.
•low grade fever, rarely rises above 38 degrees
centigrade.
swollen glands (sub occipital & posterior cervical
lymphadenopathy), joint pains, headache and
conjunctivitis.
The rash disappears after a few days with no staining or
peeling of the skin.

85. CONGENITAL RUBELLA SYNDROME
Characterized by:
Intrauterine growth restriction
Intracranial calcifications
Microcephaly
Cataracts
Cardiac defects (most commonly patent ductus
arteriosus or pulmonary arterial hypoplasia).
Neurologic disease (with a broad range of
presentations,
from behavior disorders to meningoencephalitis)
Osteitis and hepatosplenomegaly

86.  Cataract- if infection betn 3rd and 8th week of gestation.
 Deafness betn 3rd and 18th week.
 Heart abnormalities betn 3rd and 10th week.
VSD, PDA, PS, and coarctation of aorta

87. C.A.
Rubella
Primary
Infection
First Trimester
Risk of Infection-
Fetus 80%
Risk of CRS 90%
before 11 weeks
33% at 11–12
weeks
Second
Trimester
13-17 weeks
Risk of Infection-
Fetus 60%
11% at 13–14
weeks
24% at 15–16
weeks
Second
Trimester
18-20 weeks
Risk of Infection-
Fetus 25%
0%
after 16 weeks
Third
Trimester
35% at 27–30 weeks
100% beyond 36
weeks
FGR

88. 1. Since the effects of congenital rubella syndrome
vary with the gestational age at the time of infection,
accurate gestational dating should be established,
as it is critical to counselling. (II-3A)

89. Congenital defects & late manifestations of rubella infection
PRESENT AT BIRTH
1. Audiologic anomalies (60–75%)
• Sensorineural deafness
3. Cardiac defects (10–20%)
• Pulmonary stenosis
• Patent ductus arteriosus
• Ventricular septal defect
2. Ophthalmic defects (10–25%)
• Retinopathy
• Cataracts
• Microphthalmia
• Pigmentary and congenital
glaucoma

90. 4. Central nervous system (10–25%)
• Mental retardation
• Microcephaly
• Meningoencephalitis
5. Characteristic purpura
Blueberry muffin appearance
LATE MANIFESTATIONS
• Diabetes mellitus
• Thyroiditis
• Growth hormone deficit

91.  Serologic studies –
best performed within 7 to10 days after the onset of the rash and
should be repeated two to three weeks later.
 IgM Assays
 IgG Assays
 Viral isolation

92.  A fourfold rise in rubella IgG antibody titer between acute
and convalescent serum samples.
 A positive rubella-specific IgM antibody.
 A positive rubella culture (isolation of rubella virus in a
clinical specimen from the patient)

93. 2. The diagnosis of primary maternal infection
should be made by serological testing. (II-2A)

94. Samples taken
1. CVS (10-12wks of gest)
2. Amniotic fluid (14-16 weeks of gest)
3. Fetal blood (18-20 wks of gest)
PCR
Rubella-specific PCR
Advantage
Allows early detection
 CVS as early as 10-12 weeks of gestation

95.  Anomaly of CNS –Ventriculomegaly, Microcephaly, intracranial
calcifications, intra-ventricular adhesions, sub-ependymal cyst.
 Ocular abnormalities- Microphtalmia, Cataract
 Heart defects- Pulmonary artery stenosis and hypoplasia, ASD, VSD,
Cardiomegaly.
 IUGR.
 Hepatomegaly.
 Hydrops.
 Polyhydramnios.
 Ascites.
 Hyper-echogenic bowel.
 Placental enlargement.

96. Known immune ≥12 weeks of gestation.
• No further testing is necessary. CRS has not been
reported after maternal reinfection beyond 12 weeks’
gestation.
Known immune ≤12 weeks of gestation.
• If these women demonstrate a significant rise in rubella
IgG antibody titre without detection of IgM antibody, they
should be informed that reinfection is likely to have
occurred. Fetal risk for congenital infection after maternal
reinfection during the first trimester has been estimated at
8%.
• Appropriate counselling should be provided.

97. A. Gestational age ≤16 weeks.
• Acute and convalescent IgG and IgM should be obtained.
• Acute infection is diagnosed when IgM antibodies are
positive. When IgM antibodies are negative or unavailable,
testing of paired acute and convalescent sera for IgG
antibody should be performed.
• During a rubella-like illness, the acute specimen should be
drawn as soon as possible, followed by a convalescent
specimen two to three weeks later if the first IgM specimen
was negative. When there is a suspected exposure, the acute
specimen should be drawn immediately, followed by a
convalescent specimen 4 to 5 weeks later.

98. B. Gestational age between 16 and 20 weeks.
• i. Instances of CRS between 16 and 20 weeks’
gestation are rare (< 1%) and may be manifested
by sensorineural deafness (often severe) in the
newborn. Appropriate counselling to the non-
immune pregnant woman should be provided.
C. Gestational age >20 weeks.
• i. A pregnant woman exposed to rubella or
presenting with rubella-like illness after 20 weeks
of gestation should be reassured, since no studies
have documented CRS after 20 weeks.

99. D. Diagnostic difficulty–late presentation with
unknown immune status.
• i. A pregnant woman presenting 5 weeks or more after
exposure to a rash illness or 4 weeks or more after onset of a
rash presents a diagnostic dilemma.
• If IgG antibodies are negative, the patient is clearly
susceptible to rubella and has no evidence of a recent
infection.
• If IgG are positive, there is evidence of a previous infection. It
is then difficult to determine the date of infection and the risk
to the fetus, although a low level of antibody suggests more
remote infection.
• Testing for IgM antibody or repeating the test for IgG antibody
levels to determine whether there is a significant rise or
decline may be considered.

101. 3. In a pregnant woman who is exposed to rubella
or who develops signs or symptoms of rubella,
serological testing should be performed to
determine immune status and risk of congenital
rubella syndrome. (III-A)

102. The treatment of acute rubella infection is
supportive.
There are no data supporting the use of
immunoglobulin in pregnant women with acute
infection in order to diminish the fetal response to
disease.
The Centers for Disease Control recommend
limiting its use to women with known rubella
exposure who refuse pregnancy termination.

103. Universal infant immunization.
 strain- RA 27/3, live attenuated
 s/c injection

104. Febrile illness,
Immunodeficiency,
History of an anaphylactic reaction to neomycin,
Pregnancy

105.  4. Pregnancy should be avoided for 3 months following
rubella vaccination.
 5. Rubella immunization should not be administered in
pregnancy but may be safely given post partum. (III-B)
 6. Women who have been accidentally vaccinated in
early pregnancy or who become pregnant immediately
following vaccination can be reassured that there have
been no cases of congenital rubella syndrome
documented in theses situations. (III-B)

106. 1. Providing universal infant immunization to decrease
circulation of virus.
2. Using measles, mumps, and rubella or measles-rubella
vaccine as the immunizing agent in catch-up campaigns
and as the second dose in the new two-dose routine
immunization program for measles.
3. Ensuring that girls are immune before they reach child-
bearing age and using every opportunity to asses the
immunity of women of child-bearing age and providing
vaccination if necessary (pre-conceptual and infertility
consultations).

107. 4. Screening to determine the antibody status of all
pregnant women to determine susceptibility.
5. Providing programs to ensure postpartum
immunization of non-immune women before they are
discharged from the hospital.
6. Screening for immunity and vaccination, if
necessary, of all health care personnel, including
students in training.
7. Immunizing all immigrant and refugee women at
their first encounter with the Canadian health care
system, unless they have documentation of effective
vaccination or natural immunity.

108. 7. Women wishing to conceive should be counselled
and encouraged to have their antibody status
determined and undergo rubella vaccination if
needed. (I-A)

109. CYTOMEGALOVIRUS INFECTION
•A double-stranded DNA herpes virus and the most
common congenital viral infection occurring 0.5-2% of all
live births.
•The CMV seropositivity rate increases with age.
Geographic location, socioeconomic class, and work
exposure are other factors that influence the
infection.
risk of
•CMV infection requires intimate contact through saliva,
urine, and/or other body fluids.
•Possible routes of transmission include sexual contact,
organ transplantation, transplacental transmission,
transmission via breast milk, and blood transfusion (rare).

110. •Primary, reactivation, or recurrent CMV infection can
occur in pregnancy and can lead to congenital CMV
infection.
•Transplacental infection can result in intrauterine growth
restriction, sensorineural hearing loss, intracranial
calcifications, microcephaly, hydrocephalus,
psychomotorhepatosplenomegaly, delayed
development, thrombocytopenia and/or optic atrophy.
•Vertical transmission of CMV can occur at any stage of
pregnancy; however, severe sequelae are more common
with infection in the 1st trimester, while the overall risk of
infection is greatest in the 3rd trimester.

111.  Anomaly of CNS –Ventriculomegaly, intra-ventricular haemorrhage, intra-
ventricular adhesions, periventricular echogenicities, sub-ependymal cyst,
periventricular leukomalacia, microcephaly, lissencephaly, porecephaly,
cerebellar agenesis, hypogenesis, hypoplasia and haemorrhage.
 Ocular abnormalities- Microphtalmia.
 Heart defects- Cardiomegaly, pericardial effusion and calcification.
 IUGR.
 Gastrointestinal tract -Hepatomegaly, splenomegaly, echogenic bowel,
intrabdominal and liver calcification, ascites.
 Non-immunehydrops.
 Placental enlargement.

113. • The risk of transmission to the fetus in
primary infection is 30%-50%.
• Of those babies who become infected,
only 10-15% show signs of congenital CMV
after primary maternal infection.
• Of these, only 1-10% of the babies born
with the CMV infection will have symptoms
at birth and another 10-15% may not
show any symptoms at birth, but still may
have long term affects such as hearing
loss and learning disabilities.

114. DIAGNOSIS & MANAGEMENT :
•Serologic testing in women with suspected
Cytomegalovirus (CMV)
•Amniocentesis
•Ultrasonography- All above mention signs.
• Quantitative polymerase chain reaction (PCR) for viral
DNA in amniotic fluid
•Fetal magnetic resonance imaging (MRI) (considered
but not recommended)
•Intravenous treatment with CMV-hyperimmune globulin
•Ganciclovir treatment.

115. HERPES SIMPLEX VIRUS -2 INFECTION
•The most common viral sexually transmitted diseases
worldwide.
•It is a DNA virus that belongs to Alphaherpesvirinae family.
•It is most commonly found in the lumbosacral ganglia.
• It infects epithelial mucosal cells and migrate along the
nerves to reach the local-regional ganglia and persist
throughout the life of their hosts in a latent phase, may
reactivate causing recurrent infection.
•The most important HSV infection during pregnancy is the
primary genital HSV infection.

116. •Primary HSV infections in pregnant women can result in
more severe diseases than that in non-pregnant ones.
•In particular, gingivostomatitis and vulvovaginitis
herpetica tend towards dissemination. As a result, women
can develop disseminated skin lesions associated with
as hepatitis, encephalitis,visceral involvement such
thrombocytopenia, leucopoenia and coagulopathy.
• Although disseminated HSV infection is uncommon in
pregnancy, the mortality is about 50%. In particular,
pregnant women with primary mucous membrane
infection during the 3rd trimester, have an increased risk for
dissemination and they could transmit HSV to their babies
during vaginal delivery.

117. •A pregnant woman who acquires genital herpes as a
primary infection in the latter half of pregnancy, rather
than prior to pregnancy, is at greatest risk of transmitting
these viruses to her newborn.
•Additional risk factors for neonatal HSV infection include
the use of a foetal-scalp electrode and the age of the
mother < 21 years.

118. •The great majority of recurrent genital herpes is due to
HSV-2 because this virus reactivates more frequently than
HSV-1.
•Recurrent episodes of HSV infection are characterized by
the presence of antibody against the same HSV type and
the herpes outbreaks are usually mild (7–10 days) with less
severe symptoms than the first episode.
•Prodromal symptoms (itching, tingling, neuralgia) may
occur hours or days before a recurrent herpes episode.
•The apparently asymptomatic phases between clinical
outbreaks of genital herpes are important, since HSV can
reactivate periodically in latently infected cells of sensory
ganglia travelling via the neuronal axons back to the
genital mucosa, without clinical signs or symptoms. This
mechanism is known as asymptomatic virus shedding.

119. •Asymptomatic shedding has been shown to be higher in
women with HSV-2 infection.
•Although there is a small risk of vertical transmission,
recurrent genital herpes must be regarded as the most
common cause of neonatal infections and the passage
through an infected birth canal is the most probable
route of transmission .
•In recurrent infections associated with clinical symptoms,
the risk of neonatal disease is reduced dramatically by
Caesarean section.

120. Mother with
active herpes infection
(although active infection
may not be apparent)
Blisters due to
congenital
herpes
©ADAM, Inc

121. DIAGNOSIS :
•Clinical diagnosis of genital herpes is limited in accuracy.
First, HSV is only one of several diseases characterized by
genital ulcers. More importantly, many persons are
unaware that their symptoms are those of herpes.
•The typical lesions may not appear, and recurrences may
be at different locations along a dermatome. Women may
experience only prodromal symptoms, such as burning or
tingling; have single ulcers, fissures, or erosion; or
experience erythema or edema as the primary symptom.
•Available tests for herpes include both culture and PCR-
DNA testing for viral shedding, and the use of blood tests to
screen for previous exposure.

122. MANAGEMENT :
•The American Congress of Obstetricians and
Gynecologists (ACOG) recommends that women with
active recurrent genital herpes should be offered –
•Suppressive viral therapy from 36 weeks until delivery
Valacyclovir 500 mg orally BD OR
Acyclovir 400 mg orally TDS.
•Transplacental infection of the fetus is rare during
pregnancy. Intrauterine HSV infection has uncommonly
been associated with skin lesions, chorioretinitis,
microcephaly, hydranencephaly , and microphthalmia.

123. •Of greatest concern is the risk of primary infection
herpeticacquired at birth which could lead to
meningitis. The infection rate is 34 to 80% for infants born
vaginally during a primary infection.
•Cesarean section is recommended for all women in labor
with active genital lesions or prodromal symptoms such as
vulvar pain.
For patients with preterm premature rupture of membranes remote
from term complicated by recurrent maternal HSV infection, the risks of
prematurity should be weighed against the risk of neonatal HSV
disease in considering expectant management. Prophylactic
treatment with antiviral agents (eg, acyclovir) may be considered if
expectant management is chosen.

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125. REFERENCES
•Novak’sTextbook ofObstetrics – 15th edition
•TORCH Infections in Pregnancy –VeenaGupta – Jaypee
Publication – 2nd edition.
•William’sTextbook ofObstetrics – 24rd edition
•Article onTorch infections in Pregnancy –THE BRITISH
MEDICAL JOURNAL (BMJ-2013)
•Article onTORCH INFECTIONS in Pregnancy – (ACOG-2014)

126. • Ananthanarayana & Paniker’sTextbook of Microbiology 8th
edition.
• Parasitology, 13/e K. D. Chatterjee.